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Subsections
Servane Rudelle and colleagues 2007 studied the effect on weight control of a beverage containing Epigallocathechin gallate EGCG, green tea and caffeine. The authors found an increase in 24-hour energy expenditure of 100 kcal/d on account of this beverage.
The weight gain of the American population is slightly less than 1 kg/yr, which represents a median excess energy of 15 kcal/d, and because energy is stored with 50% efficiency, a negative energy balance of 100 kcal/d would be sufficient to prevent weight gain in most of the U.S. population The authors conclude that consuming this type of beverage regularly together with exercise, may be helpful in weight control.
Based on this study Nestlé and CocaCola launched its ENVIGA product with the advertising adds: Benefits: "burn more calories" "drink negative". [2]
The Federal Trade Commission (FTC) should take enforcement action against Coca-Cola and Nestlé for their unlawful deceptive advertising for Enviga, their green-tea-flavored diet soda, according to a complaint filled with the agency on May 2007 by the nonprofit Center for Science in the Public Interest (CSPI). At issue is the companies' claim that Enviga burns more calories than the five calories per can it delivers, which, CSPI says, strongly implies weight loss.
Julia Ello-Martin and colleagues 2007 assessed as reduction diet the reduction of fat in comparison to the reduction of fat together with higher intake of fruits and vegetables during 1 year.
For both groups no goals for energy or fat intake were assigned; the participants could eat ad libitum.
The low fat and high intake of fruits and vegetables group, had a lower dietary energy density,a higher weight loss (7,9 kg/1 y), and less hunger than did the low fat group (6,4 kg/1y) with variation of +- 0,9 kg for both. The authors concluded that the reduction of dietary energy density, combining increased fruit and vegetable intakes with decreased fat intake, is an effective strategy for managing body weight. Reducing fat in dairy products, convenience foods and fried products such as french fryies fish sticks, croissants, forget about oily dressings and sugar-glucose energy bars to sweeten your calories, adding fruits and vegetables to your menu is the right way.
Instead of roasting lean beef or chicken breast in your pan using plenty of oil, you can cook it using water and zero oil. Gourmet add some wine instead of water. If you add a tomato salad on vinegar you meet the Juilia Ello-Martin specifications.
Children obesity is liked to high energy intake. Olsen et al 2011 suggests that gradually reducing the amount of fat in foods for children may reduce energy consumption without reducing taste preference or liking. The authors found that reducing fat content of familiar foods, such as macaroni and cheese, pudding, chocolate milk and regular milk. Children aged between four and six, were given such foods in high-fat and in low-fat versions.
The study reports that liking and consumption by weight did not differ between high-fat and low-fat meals and the total energy intake was 59% lower for the low-fat meals. Reducing fat content is therefore being suggested by the authors to lower energy consumption of children. To increase the acceptance of lower fat in familiar traditional foods, the reduction should be processed gradually.
Reducing the use of fats and oils in the kitchen, and choosing low-fat ready to eat foods at the grocery may do a lot to avoid overweight and coronary diseases. Low-fat receipts and how to avoid fat spreads and oily sauces my be found at http://www.ourfood-news.com/Healthy_Recipes
According to Yung-hsi and colleagues 200, long-term consumption of green tea may decrease the incidence of obesity and, perhaps, green tea components such as EGCG may be useful for treating obesity. The authors point out, however, that oolong tea was found to reduce obesity in mice, despite having much less EGCG that green tea does. The authors calls for studies with purified components to identify the active components of tea.
Oolong tea [7]
According to Han and colleagues 1999 oolong tea has anti-obesity effects in high-fat diet-treated mice which might result from an enhancing effect of caffeine isolated from oolong tea The auithors suggest that oolong tea may be effective in treatment of obesity and fatty liver caused by a high-fat diet.
Effect of tea catechins on obesity [8]
Murase and colleagues 2002 studied the effects of long-term feeding with tea catechins, which are naturally occurring polyphenolic compounds widely consumed in Asian countries, on the development of obesity in mice. They found that the anti-obesity effects of tea catechins might be caused by the stimulation of the hepatic lipid metabolism They suggest that long-term consumption of tea catechins may help to suppress diet-induced obesity, and it may reduce the risk of coronary diseases. Long-term feeding of tea catechins suppressed body fat accumulation in high-fat diet-induced obesity in mice, and that their effects might be attributed, at least in part, to the activation of hepatic lipid metabolism. Consecutive intake of tea catechins (588 mg/day) reduced body fat, especially abdominal fat in humans. These results demonstrate that intake of tea catechins is beneficial for body fat accumulation.
The hPYY(3–36) has been identified to achieve weight-loss having a role in regulating appetite and energy. PYY hormone concentration in blood serum are lower in obese people during fasting and after eating, compared with lean persons.
Fazen et al 2011 used recent developments of the insulin oral delivery system as transport vehicle for PYY hormone. Added to chewing gums or oral tablets taken after a meal the B12-hPYY(3–36) conjugates described by the authors may suppress hunger for three to four hours to bridge the time gap between the meals.
Synthesis of hPYY hormone [11]
Kitagawa et al 1990 described the synthesis of the peptide synthetic hPYY was as active as synthetic porcine PYY in terms of the effects on systemic arterial blood pressure, and splanchnic blood flow.
In a 1998 review Russell-Jones describes an uptake system to overcome the hurdle of the oral administration of proteins and peptides to avoid troublesome injection. The oral route causes degradation of these products by enzymes of the digestive tract, and intestine walls provide a poor uptake by the body. In this system vitamin B12 is used to cotransport peptides and proteins through the intestine to the circulation. This technology may also be used to transport nanoparticles loaded with peptides or proteins to protect them from digestive enzymes.
Petrus, Fairchild and Doyle describe further advances on researches focused on oral peptide/protein delivery by the dietary uptake pathway for vitamin B(12), which included the delivery of erythropoietin, granulocyte-colony-stimulating factor, luteinizing-hormone-releasing hormone, and insulin. Wolfram and colleagues 2005 examined the antiobesity effect of tea epigallocatechin gallate (EGCG), in mice fed with high-fat diet.
They found that food intake was not affected but faeces energy content was slightly increased by EGCG, indicating a reduced food digestibility and thus reduced long-term energy absorption, and conclude that d ietary EGCG attenuated diet-induced body fat accretion in mice. EGCG apparently promoted fat oxidation, but its fat-reducing effect could be entirely explained by its effect in reducing diet digestibility.
Wolfram and colleagues 2005, in a study from DSM Nutritional Products Ltd found that epigallocatechin gallate (EGCG), in a pure form, present in the commercial product TEAVIGO inhibited adipocyte differentiation in vitro, and concluded that supplementation with EGCG, abolishes diet-induced obesity, and should be considered as a valuable natural treatment option for obesity.
Pei-Fang Hung and colleagues 2005 investigated the pathways of EGCG's modulation of the mitogenesis(cell- division) of preadipocytes. They found that EGCG inhibited preadipocyte 3T3-L1 proliferation.
The authors demonstrate the ERK- and Cdk2-dependent antimitogenic effects of EGCG, and that EGCG was more effective than epicatechin, epicatechin gallate, and epigallocatechin in changing the mitogenic signals. The signal of EGCG in reducing growth of 3T3-L1 preadipocytes differed from that of 3T3 fibroblasts. Hung and colleagues conclude that reduction of obesity caused by EGCG may be linked to the inhibition of fat-cells division.
Green tea catechins have been shown to promote loss of body fat and to inhibit growth of many cancer cell types by inducing apoptosis. Ji Lin and colleagues 2005 studied the influence of epigallocatechin gallate (EGCG) on adipocytes to inhibit adipogenesis and induce apoptosis using mouse 3T3-L1 preadipocytes and mature adipocytes. The researchers found that EGCG had no effect on either viability or apoptosis of preconfluent preadipocytes. EGCG also did not affect viability of mature adipocytes; however, EGCG increased apoptosis in mature adipocytes and inhibited lipid accumulation in maturing preadipocytes.
The authors concluded that EGCG can act directly to inhibit differentiation of preadipocytes and to induce apoptosis of mature adipocytes and, thus, could be an important adjunct in the treatment of obesity.
Resistin is a hormone discovered in 2001 and is a response of leucocytes to inflammation and participates in the inflammatory response, and this may be the link to insulin resistnce. According to Hang-Seng Liu and colleagues 2006 resistin is an adipocyte-specific secretory hormone that can cause insulin resistance and decrease adipocyte differentiation, and epigallocatechin gallate (EGCG) of green tea, have been reported to act against obesity and diabetes.
The study suggest that EGCG may modulate the distribution of resistin protein between the intracellular and extracellular compartments. EGCG reduced the amounts of phospho-extracellular signal-related kinase-1/2 proteins (phospho-ERK1/2 proteins). The researchers conclude that EGCG downregulates Resistin expression via a pathway that is dependent on the ERK pathway.
Resistin controversy [19]
Most all findings (many times elucidated under the same experimental conditions) reported by groups opposing the resistin link theory are the exact opposite from what those groups who support the theopry have observed. The idea that resistin links obesity to type 2 diabetes mellitus is now under even more scrutiny as recent investigations have confirmed a rather vast expression of resistin in many tissues rather than those only characteristic of obesity such as adipocytes.
With nearly as many scientists against this theory as those scientists who seem to support it, the likelihood that resistin will ever be viewed as the key node linking obesity to type 2 diabetes mellitus in the near future is very low. The very extent to which these two views oppose each other raises questions about the synchrony and methodology used in these respective groups which resulted in polar opposite results.
Wolgang, Wang an Thielecke 2006 write that studies conducted with human subjects report reduced body weight and body fat, as well as increased fat oxidation and thermogenesis related to green tea. However, according to the authors, there is still a need for well-designed and controlled clinical studies to validate the studies. According to Wolfgang and colleagues specific effects of EGCG of green tea on obesity should be investigated in human trials.
Tea-catechins together with swimming reduces obesity gain by 20 percent [3]
The effects of long-term intake of tea catechins in combination with regular exercise on the development of obesity in mice was investigated by Murase and colleagues 2006. Tea-Catechins intake in combination with swimming exercise suppressed high fat diet-induced body-weight gain by 18 and 22%, respectively, compared to Exercise and tea-Catechins intake on their own. These results indicate that intake of tea Catechins, together with regular exercise helps to reduce diet-induced obesity. This effect might be attributed, at least in part, to the activation of whole-body energy metabolism.
According to Andrews and Horvath 2008 food palatability acts on the dopaminergic reward system to override homeostatic control. The authors support the study of Ivan Araujo and colleagues 2008 which lifts questions on the dopamin theory.
The study of Araujo and colleagues used trpm5
mice which have no
capacity for sweet taste. They found that these mice developed preference
for a sugar solution based only on the caloric content and dopamin was
secreted, but not when clear water was ingested. Dopamin was not secreted when
the sugar solution was sucralose sweetener solution lacking calories.
The authors concluded that calorie-rich nutrients can directly influence brain
reward circuits that control food intake independently of palatability or
functional taste transduction. [22]
A better control of obesity could therefore be attained reducing calories content
of foods, being the taste of foods independent of the craving. This speaks for an
urgent reduction of fat, sugar and caloric load in diet to avoid overweight.
According to Kovacs and Hajnal 2008 the increased palatability of modern diet
contributes to eating beyond caloric need, adding to obesity. The authors
studied the way how palatability is coded in taste-evoked neural activity
comparing the response of brain neurons of obese and lean rat strains
triggered by different concentrations of sugar and other ingredients.
Neurons of the pontine parabrachial nucleus which relays information from the
surface of the tongue were the subject of this study. They found that the
neurons of lean rats responded to sucrose very early, while the reaction in
obese rats demanded high concentrations of sugar. Increased consumption of
sweet food could numb the reward centre of the brain reducing the intensity
of the signals which results in a weaker perception of taste through the
pontine parabrachial nucleus (PbN). The effect of other food ingredients such
as salt, water, citric acid, quinine-HCI, monosodium glutamate did not differ
between obese and lean rats.
The authors stress that fat and sugar and other sweeteners such as fructose
syrups and high intensity sweeteners, which are increasingly used in
processed foods, over-stimulate taste receptors and food reward neurons
making them less sensitive.
The authors concluded that central gustatory processing for sucrose is altered in strains of obese rat and further support the notion that
palatability is encoded in the across neuron pattern. These findings suggests
that there may be a link between taste preference and body weight affecting food intake.
Roussin and Di Lorenzo in an editorial in 2008 [24] point out that the results of the study of Kovacs and Hajnal 2008 are consistent with observations that obese humans tend
to be less responsive to mildly sweet stimuli and prefer sweeter stimuli when
compared with the nonobese, such as noted by Bartoshuk et al. 2006. Bartoshuk
added that genetic variation as well as taste pathology contribute to these results.
[25]
Roussin and Lorenzo [24], in its editorial,
reviews studies related to the perception of sweet taste stressing that obesity
may alter the taste processing of sweet stimuli at the parabrachial nucleus of
the pons (PbN) which is the home to third-order gustatory neurons and influences
the motivational and pleasure aspects of taste via dopaminergic mesolimbic
pathways.
Sweet taste does not increase caloric intake, says study [26]
Cicerale, Riddell and Keast 2012 report that taste is important to choose food, however perceived sweetness intensity alone does not influence decisively food behaviours related to sugar consumption and dietary intake in adults.
The authors studied the behaviour of 85 adults which tasted a sugar solution and rated the percepted sweetness. The study found no correlation between perceived sweetness and total caloric intake, food behaviours relating to sugar consumption dietary intake and micronutrients.
The study was based on the general labeled magnitude scale (gLMS) to measure the perceived sweetness intensity. Applying one-way analysis of variance (ANOVA) no difference between sweetness and importance of adding or not sugar to tea or coffee was found; the same results apply for avoiding sugar-sweetened or fizzy drinks. Independent t-test analysis found no association between sweetness intensity and confectionery intake, selected fruit and vegetable intake.
The authors report that persons produced similar results rating tastes and sounds using gLMS compared with magnitude matching, suggesting that the gLMS is valid for taste comparisons across nontasters, medium tasters, and supertasters.
Bartoshuk et al 2004 developed the General Labeled Magnitude Scale based on the LabeledMagnitude Scale of 1993. The gLMS is a continuous scale using "strongest imaginable of any kind" as the top rating too overcome ceiling effects. The authors explain that labeled scales use adjective/adverb intensity descriptors such as "very strong" rose odour, compared with a "very strong" headache, compressing or expanding the descriptor to fit the domain of interest.
Magnitude matching
Magnitude matching asks a person to rate the intensities of taste stimuli and stimuli of another sensory system, such as the loudness of a tone, on a similar scale to overcome different perception intensities among subjects. The sensation of taste can be categorized into five basic tastes: sweet, bitter, sour, salty, and umami.
Fat identified as sixth human taste, discovery relevant for obesity management [28]
After discovering "umami" taste, scientists postulate that fat as a "sixth taste" with CD36 receptor as responding signal to fat stimulus. CD 36 is located on the tongue and makes obese people to prefer foods with higher fat content, crave high fat foods more frequently and consume more fat than lean individuals. Pepino et al. 2011 found that CD36 genes vary among different rs1761667 genotypes (6 AA, 7 AG and 8 GG), influencing the perception of fat.
The homozygous A-allele (AA) lowers the expression of CD36. Subjects with the AA-allele had 8 fold higher detection thresholds for fat than subjects homozygous for the G-allele (GG). Heterozygous (AG) presented intermediate results. Detection threshold (sensitivity to fat) is increased by hydrolysis of triacylglycerols. Oleic acid was earlier detected than not hydrolysed fat. despite its higher viscosity.
The authors concluded that taste rather than texture is the primary detection mechanism of taste of fat, having implications in the regulation of food intake and obesity management.
Bitter taste: Bitter taste is linked to a reduction of fruits and vegetables intake in people reacting to natural bitter compounds. 6-n-propylthiouracil (PROP) a thionamide, tastes very bitter by some people, but tasteless by others depending on genetic makeup. Wooding et al. 2004 suggests that natural selection modified alleles at the PTC locus , resulting in humans."taster" and "nontaster" [29]
Saltiness: Saltiness is a taste produced by sodium, potassium or lithium.
Sourness: Sourness is a response to acidity. the taste receptor PKD2L1 is involved in this response.
Umami: The amino acid glutamic acid is responsible for umami. Some nucleotides like inosinic acid and guanylic acid enhancing the taste.
Swinburn and Eggers 2004 compares obesity with a train driving downhill.
According to the authors movement inertia, mechanical dysfunction,
psychological dysfunction, cyclical dieting, and socioeconomic disadvantage
are factors promoting weight gain, moulding an "obesogenic" environment. The
social, personal, cognitive, physiological factors which slow weight gain are
weak compared with the obesogenic ones.
In a recent study Swinburn and colleagues 2009 say that over-eating causes
obesity of developed countries. Physical activity cannot compensate the excess
calories. American adults increased the average weight by four kilograms, and
children eight kilograms during the past three decades.
According to the study adults increased weight despite having increased physical
activity. Changes in physical activity of children had no impact on growing
children obesity. To regain average weigt of people in the 70s, children should
reduce 350 calories a day (one can of soda and a small portion of French fries or
walk for an extra two-and-a-half hours a day) and adults 500 calories (one Big
Mac burger or walking two hours a day). Reducing intake is there a feasible
solution compared with a daily two hours extra walk. The authors call for a
stronger emphasis on the energy intake side than on the physical activity side.
Artham et al. 2008 st6ress that obesity is a global epidemic. It is known as a
risk of cardiovascular diseases such as heart failure, coronary heart
disease, hypertension, type 2 diabetes mellitus, dyslipidemia, certain
cancers, and chronic kidney disease. The authors found, however, that, once
these conditions develop, obese patients with hypertension, heart failure,
and coronary heart disease have a favourable prognosis.
The authors point out that greater efforts on primary prevention of obesity must
be done in the field of dietary therapy and regular physical activity.
The program was
designed to increase awareness of obesity and change the behaviours of school
children appears reduced the intake of sugary beverages and also improved body
composition in girls alone, but did not seem to affect other behaviours. The
program included lessons in biology, physical education and lifestyle changes
over eight months.
Reduction of sugary beverages were 287 millilitres per day less for boys and
249 millilitres per day less for girls and 12 months later 233 millilitres per
day less for boys and 271 millilitres per day less for girls, compared with
children of schools not participating with the program. Skinfold measures showed beneficial effects of the program as a result of reduced intake of
sugary beverages. Other behavioural measure such as consumption of snacks or
in walking or biking to school were not altered by the program.
The authors stress that reducing intake of sugar-containing beverages should
therefore be considered a good behavioural target for future interventions aimed
at the prevention of overweight among adolescents. Reduction of consumption of
sugar-containing beverages in both boys and girls should be focused in future
interventions.
Obesity, defined as a body-mass index of more than 30 kg/m2 in adults, increases worldwide. To help governments and other relevant institutions in choosing the best activities to counter the obesity epidemic, Gortmaker et al 2011 assessed quantitative models to calculate the effect of behaviours, interventions, and obesity reduction policies.
The authors found cost-effective policies that governments should prioritise to counter the obesity epidemics. To do so, governments, international organisations, the private sector, and civil society need to contribute complementary actions in a coordinated approach. However only few governments show commitment to lead obesity prevention. Activities of the food industry should be independently assessed.
The authors stress the need of policies to improve the food and built environments, cross-cutting actions such as leadership, healthy public policies, and monitoring, increase funding for prevention programmes and obesity monitoring of the population. Integration of actions within health and non-health sectors, such as trade, agriculture, transport, urban planning, and development is being considered as fundamental by the authors.
According to Rutter 2011, scientists prefer to stay within their own disciplinary boundaries. Clinicians promote clinical solutions, nutritionists support dietary ones, however, these parts must fit together and affect one another. The system must function as a whole. Tackling obesity demands to coordinate the huge number of actions of individuals, organisations, and sectors, and integrate them in a corrective system. Rutter calls to develop the understanding of complex adaptive systems, build on the biomedical paradigm, and move beyond linear thinking to create new ways to tackle obesity or other problems, such as climate change. [35]
To predict the bodyweight time course the dynamic energy imbalances must be considered. Hall and colleagues 2011describe a mathematical model to simulates energy expenditure adaptations during weight loss, and a web-based simulator for prediction of weight change dynamics.
The authors found that bodyweight response to a change of energy intake is slow, with half times of about 1 year, adults with greater adiposity have a larger expected weight loss for the same change of energy intake, and to reach their steady-state weight will take longer than it would for those with less initial body fat.
Calculating the energy-balance dynamics of the US adult obesity epidemic Hall and colleagues found that a persistent average daily energy imbalance gap between intake and expenditure of about 30 kJ per day caused the average weight gain of the US population. However, energy intake rose to about 0,9 MJ per day in order to compensate the increased expenditure associated with increased weight. This is needed to reverse the obesity epidemic.
Health and nutrition organisations have created the believe that a reduction of food intake of 2 MJ per day will lead to a steady rate of weight loss of 0,5 kg per week. This is a static weight-loss rule which does not consider the dynamic physiological adaptations that occur with decreased bodyweight. It leads to drastically overestimated expectations for weight loss says Hall and colleagues.
The dynamic simulation model of adult human metabolism, developed by Hall, predicts the time course of individual weight change in response to behavioural interventions. The authors suggest as a rule of thumb for an average overweight adult that every change of energy intake of 100 kJ (25 Cal) per day will lead to an eventual bodyweight change of about 1 kg with half of the weight change being achieved in about 1 year and 95% of the weight change in about 3 years.
Three hydrocolloid coating materials were tested in reducing fat uptake in battered fish products. Camden and Chorleywood Food Research Association Group coatings such as alginate, pectin, gellan gum, methyl cellulose, and hydroxypropyl methyl cellulose. Fish fillets were coated with alginate, pectin and gellan gum and then fried. All three coated battered fish fillets with either water or one of the three hydrocolloids showed reduced fat level in the final product.
These findings could help to reduce total lipid intake by the population as fried fish is an important constituent of the average population.
The authors suggest that the reduction of fat was due to the waterbinding ability of the coatings. In fully fried products, the reduction in fat uptake was less marked, although an effect was still seen.
It is likely that the longer frying times compromised the integrity of the coatings, emphasising the need to consider the requirements of both product and process when applying edible films.
Unhealthy diets and lack of physical activity are the leading causes of avoidable illness
and premature death in Europe, and the rising prevalence of obesity across Europe is a
major public health concern.
The Green Paper of the Commission of the European Communities entitled" Promoting healthy diets and physical activity: towards a European strategy for the prevention of overweight, obesity and chronic diseases" opens the discussion on the obesity crisis, focusing on the factor of food for the prevention of chronic diseases, overweight and obesity
Improving the health of Europeans through better diets and greater physical activity is crucial to preventing a range of non-communicable diseases and improving quality of life for millions of people.
According to the Confederation of Food and Drink Industry of the EU a greater understanding of all obesity-related factors is needed, calling for improved public health education on nutrition and healthy lifestyles. This would enable consumers to take responsibility for making healthy choices. It will be also be the basis for understanding and making use of product information provided by the industry.
Strategies should include the determinants that affect food choice, factors that lead to insufficient physical activity in every-day life, and not just food products themselves. [38]
The Green Paper considers industry self-regulation the best way of dealing with the problem. According to the CIAA, however, a broader approach is needed to meet all factors involved, such as:
- It should be clear that each consumer is responsible for ensuring that his or her own lifestyle is a healthy one.
- Parents have a similar responsibility for their children.
- Increase of level of physical activity in children, adolescents and adults, in particular in the school environment.
The European Vending Association (EVA) questions the scientific data of the Green Paper regarding the excessive intake of energy-dense snacks and sugar-sweetened soft drinks:
EVA says the "notion of excessive intake" is vague and very subjective, and it is unclear how it impacts directly on the Body Mass Index. EVA calls for other factors such as energy out determining if intake is excessive or not.
The classic diets and fasting are seldom long lasting. The pharmaceutical industry is conscious of the growing market of drugs to reduce weight without changing once life habits.
H. HAUNER [40] writes:"For the moment being there are no convincing drugs for treatment of overweight. The majority of authorized Drugs act on the neurotransmitter noradrenalin or serotonin.
Suppressant of appetite like derivates of amphetamines should be used very seldom because of their side reactions (such as rise of heart beat frequency and rise of blood pressure, insomnia, pulmonary hypertension), their short time of activity and the danger of habit formation.
A long-time effect every overweight therapy are disappointing. Only less than one third of patients can hold their weight after a diet." [41] [42] Antiobesity treatment is recommended for selected patients in whom lifestyle
modification is unsuccessful. In US there are only two antiobesity drugs
licensed. Orlistat is a gastrointestinal lipase inhibitor, reduces
weight and decreases progression to diabetes in high-risk patients; adverse
gastrointestinal effects are common. Orlistat works by inhibiting pancreatic
lipase, an enzyme that breaks down triglyzerides in the intestine into absorbable
free fatty acids. Fat is excreted undigested.
Orlistat is a synthetic substance resulted from the research regarding lipstatin which had been found in bacteria which live in the soil of Mallorca, the Island in the Mediterranean Sea. Lipstatin was found to slow down the absorbtion of fat. This took the research of Roche to the discovery of orlistat. Xenical was liberated on the European market in august 1998. Tam, Lecoultre and Ravussin 2011 point to the fact that there are currently no treatment options for obesity. Many drugs were removed from the market due to significant side effects, such as Sibutramine. Orlistat provide only modest weight loss. The promising combination of leptin/amylin in the form of pramlintide/metreleptin, for the treatment of obesity in a randomized clinical trial was stopped due to safety concerns. Pramlintide is an analog of the hormone amylin.
These trials were based on the study of Roth et al.2008 which explained that body weight is regulated by the interactions between endocrine signals of long-term adiposity, such as leptin, a hypothalamic signal, and short-term satiety, such as amylin, a hindbrain signal. The authors report a synergistic effect of fat-specific weight loss when amylin and leptin is given to leptin-resistant diet-induced obese rats. [44] Sibutramine has the generic name Merida in Europe and Reductil in US. It is a monoamine-reuptake
inhibitor which results in weight losses, but is associated with increases in
blood pressure and pulse rate. Sibutramine acts by increasing serotonin and
norepinephrine levels in brain. The serotonergic action, in particular, is
thought to influence appetite. Rimonabant is the first of the endocannabinoid receptor
antagonists, reduces weight and improves waist circumference and concentrations
of HDL cholesterol and triglyceride. It works by blocking the CB1 receptors in the brain.
In Europe, it is indicated for use in conjunction with diet and exercise for
patients with a body mass index greater than 30 kg/m²or patients wih a BMI
greater than 27 kg/w² with associated risk factors, such as type 2 diabetes
or dyslipidaemia.
However, an increased incidence of mood-related disorders has been reported.
Generic names are Acomplia in Europe, and Riobant, Slimona, Rimoslim in India.
In United States, it is intended to be marketed under the name Zimulti.
The FDA concluded in 2007 that Sanofi-Aventis failed to demonstrate the safety
of rimonabant and voted against recommending the anti-obesity treatment for
approval. The main concern was over suicidality, depression and other related
side effects associated with use of the drug.
Anti-obesity drug Acomplia: German health insurance does not pay
for acomplia and scientist warns for late-effects [45]
The Lower House of the German Parliament (Bundestag) decided that German health insurance will not pay for Acomplia classifying the drug as lifestyler.
Rimonabant is the active ingredient of Acomplia. The drug
was banned in USA because of depression and suicide side effects, but is
approved in France, Germany and UK. [46]
Acomplia acts on the central nerve system, blocking certain receptors. This is
of concern for the neurobiologist Andreas Zimmer from the University Bonn,
Germany. He found that a special type of mice which received Acomplia had a
reduced lifespan, presented epilepsy and a loss of nerve cells in the brain was found.
The producer of the drug, Sanofi-Aventis, argues that effects in animals cannot
be translated to human physiology. Zimmer says that the 2 an 3 years studies
presented by Sanofi-Aventis were to short to show late-effects. The company
expects revenues from Acomplia of up to 5 billion Dollar/year. It is an antidepressant which is also licensed
for bulemia nervosa and is therefore sometimes classified as antiobesity drug.
Other antiobesity drugs acting on the central melanocortin pathway, are far
away from clinical use.
A meta-analysis of trials by the international Cochrane Collaboration
concluded in 2007 that in diabetic patients Fluoxetine, orlistat, and
sibutramine can achieve statistically significant weight loss over 12 to 57
weeks. The magnitude of weight loss is modest, however, and the long-term
health benefits remain unclear. The safety of sibutramine is uncertain. There
is a paucity of data on other drugs for weight loss or control in persons with
type 2 diabetes. [47]
Raj S. Padwal and colleague criticise all antiobesity drug trials because they
have been limited by their high attrition rates and lack of long-term morbidity
and mortality data. The authors suggest that the assessment processes of new
antiobesity drugs should include both surrogate endpoints such as weight loss,
and clinical outcomes such as major obesity-related morbidity and mortality, to
insure that the putative benefits of such drugs outweigh their risks and costs.
[48]
Xenical is a drug containing the substance orlistat . It can reduce bodyweight up to 10% without serious side effects.
Xenical can help when used for a long period together with a change of life habits. Its activity takes place in the intestines. It reduces the absorption of fat up to 30 percent. Xenical is being produced by Hoffmann la Roche, Grenzach, Swiss. A large number of studies tried to tackle the obesity problem. Creatine ignites new hopes in treating lipid diseases. Supplementation of 1% (wt:v) of creatine monohydrate to the liquid high-fat diet with 71% calories derived from fat was found by Deminice et al.2011 to reduce fat accumulation in liver of rats.
Pathologic increases of liver parameters such as cellular oxidative stress, immunity and other liver function linked parameter were improved, compared with rat under this diet but without supplementation of creatine.
The authors suggest that high-fat diet decreased mRNA for PPARalfa as well as 2 of its targets, carnitine palmitoyltransferase and long-chain acylCoAa dehydrogenase. Creatine supplementation normalized these mRNA levels preventing the formation of fatty liver.
Johnston and Gaas 2006 write that scientific investigations do not support the
use of vinegar as an anti-infective agent, reduced risk for hypertension and
cancer.
Vinegar ingestion, however, reduces postprandial responses of blood glucose
and insulin, and increased satiety. Ostman and colleagues 2005 point to thr
potential of fermented and pickled products containing acetic acid.
[51]
Future investigations,however, are needed to explain how vinegar alters
postprandial glycemia and to determine whether regular vinegar ingestion
favourably influences glycemic control. Johnston and Gaas calls for more
studies to determine whether vinegar is a useful for the therapy of diabetes
or prediabetes.
Kondo and colleagues 2009 studied the effect of 0.3 or 1.5% acetic acid on
the prevention of obesity in high-fat-fed mice. The administration inhibited
the accumulation of body fat and hepatic lipids without changing food
consumption or skeletal muscle weight.
The authors suggest that weight reduction where due to the effect of the acetic
acid increasing fatty oxidation and thermogenesis in the liver through
PPAR-alpha. The acetic acid upregulated the expression genes for PPAR-alfa and
fatty-acid-oxidation-related enzymes in the liver. [52]
Amphetamines were used in war to keep soldiers awake during combat.Later amphetamines were found to act as appetite suppressant and being sold as such. Very soon the selling was canceled because of heart complaints, Angina-pectoris tremble and nervosity.
Phentermine is the active substance of Adipex N and norephedrine
was used in Antidiapositum X 112 Fugoa N and Regenon. They are appetite suppressant. They have the same side reactions noted by amphetamines. Phentermin was prohibited in Germany because of the high blood pressure of the pulmonary artery. In Austria it is still being sold under the name Adipex.
Aminorex was used as active substance of the drug Menocil. Its selling was canceled because of irreparable high pressure at the pulmonary artery.
Phenfluramine is an appetite suppressant which stimulates serotonin presenting the same side reactions described above as well as depressions. Researches
at the Osaka University of Pharmaceutical Sciences and Taiwanese researchers have demonstrated vasodepressing properties which help to control high blood pressure.
Sesamin, a supplement made from sesame exerts action on nitric oxide production and its ability to inhibit ET-1 production from endothelial cells. ET-1 constricts blood vessels.
A combination of the dopamine and norepinephrine reuptake antagonist bupropion
and the opioid antagonist naltrexone were proposed to treat obesity. The dual
mechanism of action is to stimulation of central melanocortin pathways,
resulting in increased energy expenditure and reduced appetite. Contrave of
Orixegen will be approved by FDA in a combination of 360 mg bupropion and 32
mg naltrexone in a single tablet. [53]
The recommended daily dose of Contrave is two 8mg naltrexone/90 mg bupropion
tablets taken twice daily (4 tablets total - 32 mg naltrexone, 450 mg
bupropion). Upon initiation, the drug will be started with a quarter-dose (or
one tablet) for one week and a pill will be added to the regimen each week
until the full recommended dose is reached on Week 4. Treatment is designed to
affect the hypothalamus to decrease food intake over extended period of time.
[54]
The US Food and Drug Administration Endocrinologic and Metabolic Drugs
Advisory Committee gave a positive recommendation for the use of Contrave in
the treatment of obesity and weight management. The final approval is expected
for Jan 31, 2011. Its use may produce a decrease in bodyweight of 5
percent. But this drug showed weight loss only when combined with lifestyle
modification. The underlying causes of obesity must also be addressed such as promoting the modifications of lifestyle, diet, and exercise.
[55]
Hypothalamic melanocortins, particularly alpha-MSH, are known to constitute the
main brake to consumptive behaviour of food. Opiates are known to both
suppress alpha-MSH and to stimulate hedonic food consumption, therefore the
antagonism between melanocortins and opioids are promising to reduce obesity.
Monoamines, opioids and cannabinoids are known to be involved in appetite
regulation acting on the hypothalamic appetite regulatory centre, more studies
on this subject are being suggested by Reece 2010. [56]
The Contrave Obesity Research I (COR-I) study assessed the effect of
naltrexone and bupropion treatment on bodyweight in overweight and obese
participants. The adverse event were nausea, headache, constipation,
dizziness, vomiting, and dry mouth. A transient increase of around 1.5 mm Hg
in mean systolic and diastolic blood pressure was followed by a reduction of
around 1 mm Hg below baseline. No increase of depression or suicidality
events compared with placebo were noted. [57]
Nathan and colleagues 2008 stress that antiobesity drugs target the central
neurochemical systems including the monoamine, opioid, and cannabinoid systems
which also modify emotional behaviour and cognitive function, acting on the
receptors within the fronto-striatal and limbic circuitry. Drugs targeting the
m-opioid receptors, such as naltrexone and combination therapies targeting the
opioid and monoamine systems, such as Contrav were reported to produce sedfation
and tiredness. The authors recommend, therefore, to assess assess
neuropsychiatric adverse events antiobesity drugs with such central mechanism of
action. [58]
According to Tim J. Schulz and colleagues 2010, brown fat cells are specialized
for energy expenditure and may be included in a strategy for body weight reduction. The
authors found that progenitor cells in mouse white fat tissue and skeletal
muscle (Sca-1(+)/CD45(-)/Mac1(-), referred to as Sca-1(+) can be transformed
into brown fat cells.
The authors report that fat cells, marked with Scal protein and exposed to BMP-7 protein, presented characteristics of brown fat cells. The differentiation
could be intensified by adding rosiglitazone, known as a diabetes drug. The
molecular characteristics of tissue-resident adipose progenitors were determined
by the group around Schulz.
The authors stress that diet and exercise are still the best approaches for
losing weight in the general population. Therapy involving energy-burning brown
fat cells may, however, help people with heavy body weight problems.
According to Perfield et al.2011 tumor progression locus 2 (TPL2), a kinase that integrates signals from Toll receptors, cytokine receptors, and inhibitor of K-B kinase-beta mediates obesity-associated inflammation and insulin resistance.
Mice fed with a low-fat diet or a high-fat diet to investigate the effect of TPL2 deletion on obesity, inflammation, and insulin sensitivity. The authors found that TPL2 deletion does not alter body weight gain or adipose depot weight, but improves insulin sensitivity with enhanced glucose uptake in skeletal muscle and increased suppression of hepatic glucose output, diminished immune cell infiltration reduced inflammation in obese TPL2-suppressed mice. The author concluded that TPL2 is a target which may improve the metabolic state associated with obesity.
Supplementation of a high-fat diet with whole blueberry powder of Vaccinium ashei and Vaccinium corymbosum was found by DeFuria et al. 2009 to protects against adipose tissue inflammation and insulin resistance but did not alter energy intake, metabolic rate, body weight, or adiposity. The authors report that the shift toward global upregulation of inflammatory genes, increased M1-polarized ATMPhi (CD11c+), and increased oxidative stress was attenuated or nonexistent in mice fed with blueberries which were also protected from insulin resistance and hyperglycemia adipocyte death. These effects may result from anthocyanins of blueberries which alter mitogen-activated protein kinase and nuclear factor-kappaB stress signaling pathways.
According to Perfield 2011 abnormally high belly fat or abdominal adiposity has been linked to a range of health problems, including insulin resistance, diabetes, cardiovascular disease and other obesity-associated health disorders. The author found that oil of the seeds of the Sterculia foetida tree contains sterculic oil curbs a human enzyme associated with insulin resistance. Belly fat is a key to reducing the incidence of serious disease, and this oil could have a future as a nutritional supplement. Mice with high amount of abdominal fat, which were fed with sterculic oil, presented decreased liver fat and an improved glucose tollerance. The dose was comparable to providing 3 grams of sterculic oil to a 250 pound human.
Malvalic acid and sterculic acid are cyclopropene fatty acids.
The structure of sterculic acid was proposed by Nunn as C19 H34 O2, by the method of urea complexes and suggested its structure as omega-(2n-octylcycloprop-1-enyl)-octanoic acid (I). [63]
Sterculic acid is present in sterculia oils and at 12% in kapok seed oil, cottonseed oil 1%and in the seeds of the tree Sterculia foetida 65-78%. The authors stress that these acids are highly reactive and are destroyed during refining and hydrogenation of the oils. [64]
Asp et al. 2011 reported that a daily dose of 8g of safflower oil for 16 weeks may improve glycemia, inflammation, and blood lipids in obese postmenopausal women who have Type 2 diabetes. No such effects were noted with conjugated linoleic acid.
Miyoshi et Al. 2010 describe the function of perilipin A in adipocyte lipid droplets which is essential for lipid storage and lipolysis. Overexpression of perilipin diminished adipose tissue, elevates basal lipolysis, reduces catecholamine-stimulated lipolysis, and increased insulin resistance, lower body weight, fat mass, and adipocyte size were also attained. The expression of oxidative genes was increased and lipogenic genes decreased in brown adipose tissue of transgenic mice.
Sawada and colleagues 2010 report that FSP27 has been shown to control gene expression of fat metabolic regulators. Overexpression of Perilipin A in 3T3-L1 adipocytes also reduced FSP27 expression and diminished lipid droplet size. The authors concluded that overexpression of Perilipin A in white adipocytes reduces lipid droplet size by decreasing FSP27 expression and thereby inducing a brown adipose tissue-like phenotype. The authors suggest to modulation the lipid droplet proteins in white adipocytes as a treatment of obesity and its related disorders. [67]
Souza et al. 2007 reports that protein kinase A-mediated perilipin phosphorylation is essential for norepinephrine-dependent lipolysis and thermogenesis in brown adipose tissue . The authors report that in perilipin knockout mice an increased basal lipolysis attributable to the absence of perilipin causes a temperature increase of approximately 3.0 degrees C, suggesting that. one or more norepinephrine-dependent mechanism of perilipin phosphorylation regulates the interscapular brown adipose tissue thermal response. [68]
Sensing of extracellular calcium by CasR is important in regulating calcium homeostasis,The CasR has a predominant role in controlling parathyroid gland function. CasR receptor also has functions in other tissues, including regulation of renal calcium excretion and calcitonin secretion by thyroidal C-cells, but sensing mechanisms for extracellular calcium in other tissues outside of the parathyroid gland, kidney, and thyroidal C-cells is unclear.
He et al 2011 report that low-calcium intake is associated with increased risk of obesity. The calcium-sensing receptor (CaSR) plays an important role in modulating the expression of rate-limiting lipolysis enzymes in human adipocytes. Rats fed with a low-calcium diet had greater visceral fat mass, lower serum FFA and glycerol concentrations, and greater CaSR expression in white adipose tissue than did those fed with normal-calcium. The authors suggest that low-calcium diet affects the CaSR pathway with antilipolytic activity leading to obesity.[70]
The calcium-sensing receptor (CaSR) was found by He et al. to maintaining constant blood Ca(2+) levels and has an inhibitory effect on lipolysis by mediating potential [Ca(2+)](i) and cAMP pathways. [71]
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