Effect of weight loss by a low-fat diet and a low-carbohydrate diet on peptide YY levels

Essah, Paulina A.; Levy, James R.; Sistrun, Sakita N.; Kelly, Susan; Nestler, John E.

doi:10.1038/ijo.2010.48

Cited by 48 publications

(49 citation statements)

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“…In general, if these signals change in the obese humans in response to energy-restricted weight loss, a collective signal favoring hunger over satiety/satiation is observed (Table 1). However, detection of this adaptive response is much less consistent than that of circulating adipose signals and nutrients, as they may be dependent on the presence of a negative energy balance (2,30,42,71,133), the amount of weight loss (71), the amount of physical activity (121), the specific derivative of the hormone measured [peptide YY(PYY) vs. PYY3-36; total vs. acetylated ghrelin] (18) or the type of macronutrient restricted in the diet (71,95). Even under the same conditions of weight loss and maintenance, there is a wide variability in individual responses with respect to these adaptations in hunger and satiety signals (18).…”

Section: The Gut: Sensing the Prandial Statementioning

confidence: 99%

Biology's response to dieting: the impetus for weight regain

MacLean

Bergouignan

Cornier

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

369

326

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Dieting is the most common approach to losing weight for the majority of obese and overweight individuals. Restricting intake leads to weight loss in the short term, but, by itself, dieting has a relatively poor success rate for long-term weight reduction. Most obese people eventually regain the weight they have worked so hard to lose. Weight regain has emerged as one of the most significant obstacles for obesity therapeutics, undoubtedly perpetuating the epidemic of excess weight that now affects more than 60% of U.S. adults. In this review, we summarize the evidence of biology's role in the problem of weight regain. Biology's impact is first placed in context with other pressures known to affect body weight. Then, the biological adaptations to an energy-restricted, low-fat diet that are known to occur in the overweight and obese are reviewed, and an integrative picture of energy homeostasis after long-term weight reduction and during weight regain is presented. Finally, a novel model is proposed to explain the persistence of the "energy depletion" signal during the dynamic metabolic state of weight regain, when traditional adiposity signals no longer reflect stored energy in the periphery. The preponderance of evidence would suggest that the biological response to weight loss involves comprehensive, persistent, and redundant adaptations in energy homeostasis and that these adaptations underlie the high recidivism rate in obesity therapeutics. To be successful in the long term, our strategies for preventing weight regain may need to be just as comprehensive, persistent, and redundant, as the biological adaptations they are attempting to counter. energy restriction; diet-induced obesity; obesity prone; weight loss; energy balance IN THE UNITED STATES, OVER 60% of adults and close to 20% of children are overweight or obese (35,174). A number of effective weight loss strategies are available, but most are only transiently effective over a period of 3 to 6 mo. Less than 20% of individuals that have attempted to lose weight are able to achieve and maintain a 10% reduction over a year (128). Over one-third of lost weight tends to return within the first year, and the majority is gained back within 3 to 5 years (3,246). A number of reasons have been proposed for the high incidence of weight regain (69,246), and several point to the biological response to weight loss.The objective of this review is to examine the role of this biological response in the process of weight regain. Biological regulation is first discussed in relation to other nonbiological pressures that affect body weight as weight is gained, lost, and regained. The specific biological adaptations to the most common form of dieting, an energy-restricted low-fat diet, are then discussed in more detail. Previous reviews provide extensive descriptions of the normal adaptive response to energy restriction. We do not attempt to recapitulate those efforts here. Rather, the unique perspective of this review summarizes those adaptations that have been confirmed o...

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Section: The Gut: Sensing the Prandial Statementioning

confidence: 99%

Biology's response to dieting: the impetus for weight regain

MacLean

Bergouignan

Cornier

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

369

326

View full text Add to dashboard Cite

show abstract

“…Of note, changes in leptin with weight loss have been shown to be predictive of weight regain and may therefore represent a key modulator of weight regain [21]. Gut-derived peptides such as ghrelin, PYY, and GLP-1 play important roles in the short-term meal-to-meal signaling of appetite and are also altered by weight loss, favoring and predicting increased food intake [21][22][23][24][25]. Gut peptide responses to weight loss, however, are variable likely due individual responsiveness to meals (macronutrients, fiber content, size), and thus may be a more or less important adaptive mechanism [25].…”

Section: Changes In Appetite-related Peripheral Signalsmentioning

confidence: 99%

Is your brain to blame for weight regain?

Cornier

2010

Appetite

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“…124 Short-term gut-related peptides such as ghrelin, PYY, and GLP-1, which play important roles in the meal-tomeal signaling of appetite, are altered by weight loss, favoring increased food intake. [125][126][127][128] Recently, neuroimaging studies have shown that the weight-reduced state is associated with enhanced signaling in the motivation, reward, attention, and behavioral centers of the brain 129 -131 and that these brain responses respond to physiological signals such as leptin. 132 In summary, although caloric restriction results in shortterm weight loss, it is extremely difficult for individuals to maintain this weight loss over the long term.…”

Section: Changes In Energy Intakementioning

confidence: 99%

Prevention of Overweight/Obesity as a Strategy to Optimize Cardiovascular Health

et al. 2011

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he prevalence of obesity in the United States and the world has risen to epidemic/pandemic proportions. This increase has occurred despite efforts by healthcare providers and consumers alike to improve the health-related behaviors of the population and a tremendous push from the scientific community to better understand the pathophysiology of obesity. This epidemic is all the more concerning given the clear association between excess adiposity and adverse health consequences such as cardiovascular disease (CVD) and type 2 diabetes mellitus (T2DM). These risks associated with overweight/obesity are primarily related to the deposition of excess adiposity or body fatness. Weight loss, specifically loss of body fat, is associated with benefits in all of the obesity-related comorbidities, but, unfortunately, most weight loss interventions are associated with weight regain and are therefore not successful in the long term. It is for these reasons that efforts to prevent weight gain and overweight/ obesity are necessary. This is especially important when one considers younger individuals, who have even more to lose as a consequence of a longer duration of excess adiposity.After a brief review of the epidemiology of obesity, this statement will make the case for the importance of weight gain prevention. This argument will first include a review of the complications of overweight and obesity in both adults and children, including the future CVD risks of obesity in early life. Energy balance dysregulation and adaptations to the weight-reduced state, favoring weight regain, will then be reviewed as further argument for the need for obesity prevention. This will be followed by a discussion on the goals and strategies for accomplishing the difficult task of the prevention of weight gain and obesity. Scope of the Problem Classification of Overweight and ObesityThe body mass index (BMI) is the most widely used and accepted method for the assessment and classification of excess adiposity or body fatness. Overweight and obesity are classified according to BMI for adults. 1 A BMI Ͻ18.5 kg/m 2 is considered underweight, between 18.5 and 24.9 kg/m 2 corresponds to a healthy weight, between 25.0 and 29.9 kg/m 2 is overweight, and Ն30.0 kg/m 2 is obese. Obesity is further classified as stage I or mild (BMI of 30.0 to 34.9 kg/m 2 ), stage II or moderate (BMI of 35.0 to 39.9 kg/m 2 ), and stage III or severe (BMI of Ն40.0 kg/m 2 ). In children, BMI percentiles adjusted for age and sex and calculated on the basis of a compilation of national survey data collected over a 30-year period are used. In children aged 2 to 19 years, overweight is defined as a BMI between the 85th and 95th percentiles, and obesity is defined as a BMI Ն95th percentile. 2 Epidemiology of Overweight and ObesityThe prevalence of overweight and obesity in the United States and the world has risen dramatically over the last 4 to 5 decades and has been summarized. 3,4 In the most recent US population estimates based on data from the 2007-2008 National Health and Nutri...

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Effect of weight loss by a low-fat diet and a low-carbohydrate diet on peptide YY levels

Cited by 48 publications

References 11 publications

Biology's response to dieting: the impetus for weight regain

Biology's response to dieting: the impetus for weight regain

Is your brain to blame for weight regain?

Prevention of Overweight/Obesity as a Strategy to Optimize Cardiovascular Health

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