Metabolic Defense of the Body Weight Set Point

Keesey, Richard E.; Corbett, Stephen W.

doi:10.3928/0048-5713-19831101-03

Cited by 26 publications

(30 citation statements)

References 8 publications

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“…The fact that BMI was related to Physical and psychological scores of subjects who underwent a diet intervention "sometimes" (n = 21) or "often" (n = 30) before the present study. *Three factor eating behavior questionnaire **Eating disorder examination questionnaire ***Dutch eating behavior questionnaire weight regain might be explained by the set point theory (12,24,25). Kramer and colleagues (12) thoroughly discussed the biological model of BW set point (and thus BMI set point, because the height remains the same), as an alternative explanation for maintenance failure.…”

Section: Discussionmentioning

confidence: 99%

Predictors of Weight Maintenance

Pasman¹,

Westerterp-Plantenga²

1999

Obesity Research

170

123

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PASMAN, WILRIKE J., WIM H.M. SARIS, AND MARGRIET S. WESTERTERP-PLANTENGA. Predictors of weight maintenance. Obes Res. 1999;7:43-50. Objective: To obtain predictors of weight maintenance after a weight-loss intervention. Research Methods and Procedures:An overall analysis of data from two-long intervention studies [n = 67 women; age: 37.9±1.0 years; body weight (BW): 87.0±1.2 kg; body mass index: 32.1±0.5 kg-m<"; % body fat: 42.4±0.5%]. Subjects were measured before a very low energy diet (month 0), after the very low energy diet of 2 months (month 2) and after a 14-month follow-up phase (at 16 months), in which fiber or a carbohydrate-containing food supplement was supplied. The baseline measurements and the changes in parameters induced by the diet intervention were used to predict the changes in BW in the follow-up phase [dBW(2-16)].Results: Multiple regression analysis revealed that 50% (p<0.001) of the variability in weight regain could be explained by pphysiological and behavioral factors. These were: frequency of previous dieting (? = 0.27, p<0.05), hunger score (measured with the three-factor eating behavior questionnaire), and change in 24-hour resting metabolic rate (RMR). Frequent dieters showed significantly more weig~t regain than less frequent dieters (8.8± 1.0 kg vs. 5.1 ±0.8 kg, p

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Section: Discussionmentioning

confidence: 99%

Predictors of Weight Maintenance

Pasman¹,

Westerterp-Plantenga²

1999

Obesity Research

170

123

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“…The network of brain areas containing these metabolic sensors forms a distributed network that functions as an integrated system. Thus the early observations that destruction of the VMH or LHA leads to marked disturbances in energy and glucose homeostasis (209,210,240,241,341,534) do not mean that these are satiety and feeding centers; it simply means that destroying one node of this distributed network can lead to dysfunction of its integrated function. While there is a great deal of redundancy in this distributed network, many of its component parts can undergo plasticity, particularly during early pre-and postnatal development through alterations in neural connections and expression of neuro-transmitters and -peptides (58, 59, 62, 98, 391-393, 490).…”

Section: B Metabolic Sensing Neurons: the Basic Integrators And Regumentioning

confidence: 99%

Gene-Environment Interactions Controlling Energy and Glucose Homeostasis and the Developmental Origins of Obesity

Bouret

Levin

Ozanne

2015

Physiological Reviews

137

103

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LBouret S, Levin BE, Ozanne SE. Gene-Environment Interactions Controlling Energy and Glucose Homeostasis and the Developmental Origins of Obesity. Physiol Rev 95: 47-82, 2015; doi:10.1152/physrev.00007.2014.-Obesity and type 2 diabetes mellitus (T2DM) often occur together and affect a growing number of individuals in both the developed and developing worlds. Both are associated with a number of other serious illnesses that lead to increased rates of mortality. There is likely a polygenic mode of inheritance underlying both disorders, but it has become increasingly clear that the pre-and postnatal environments play critical roles in pushing predisposed individuals over the edge into a disease state. This review focuses on the many genetic and environmental variables that interact to cause predisposed individuals to become obese and diabetic. The brain and its interactions with the external and internal environment are a major focus given the prominent role these interactions play in the regulation of energy and glucose homeostasis in health and disease.

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“…However, in obese individuals the 'set-point' or 'settling-point' about which they are balanced tends to rise throughout life and, at each successively higher level, cannot be lowered permanently by any conventional therapy in the majority of individuals (Scarpace et al 2000a,b). There is a controversy about whether body weight and adipose stores are actually regulated variables (Wirtshafter & Davis 1977;Davis & Wirtshafter 1978;Stunkard 1982;Keesey & Corbett 1984;Flatt 2000). Regardless, of whether these are actively or passively regulated, it is clear that specific levels are actively defended when attempts are made to drive them off a given baseline.…”

Section: Introductionmentioning

confidence: 99%

“…One possibility is that neuronal plasticity occurs within the central nervous systems with formation of new neural connections much as occurs during the formation of long-term memories (Levin & Keesey 1998;Levin 2000). While evidence for such naturally occurring, permanent changes in neural connectivity are lacking, a variety of lesions within the complex network of neurons and metabolic sensors within the brain and periphery can markedly and permanently alter the level about which body weight is defended (Mitchel & Keesey 1977;Keesey & Corbett 1984;Vilberg & Keesey 1984King et al 1993a,b;Bellinger & Bernardis 2002). Thus, a variety of alterations in the connectivity and function of pathways regulating energy homeostasis, whether naturally occurring or experimentally imposed, can lead to major changes in the level of defended body weight and adiposity.…”

Section: Introductionmentioning

confidence: 99%

Metabolic imprinting: critical impact of the perinatal environment on the regulation of energy homeostasis

Levin

2006

Phil. Trans. R. Soc. B

200

170

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Epidemiological studies in humans suggest that maternal undernutrition, obesity and diabetes during gestation and lactation can all produce obesity in offspring. Animal models have allowed us to investigate the independent consequences of altering the pre-versus post-natal environments on a variety of metabolic, physiological and neuroendocrine functions as they effect the development in the offspring of obesity, diabetes, hypertension and hyperlipidemia (the 'metabolic syndrome'). During gestation, maternal malnutrition, obesity, type 1 and type 2 diabetes and psychological, immunological and pharmacological stressors can all promote offspring obesity. Normal post-natal nutrition can reduce the adverse impact of some of these pre-natal factors but maternal high-fat diets, diabetes and increased neonatal access to food all enhance the development of obesity and the metabolic syndrome in offspring. The outcome of these perturbations of the perinatal environmental is also highly dependent upon the genetic background of the individual. Those with an obesity-prone genotype are more likely to be affected by factors such as maternal obesity and high-fat diets than are obesity-resistant individuals. Many perinatal manipulations appear to promote offspring obesity by permanently altering the development of central neural pathways, which regulate food intake, energy expenditure and storage. Given their strong neurotrophic properties, either excess or an absence of insulin and leptin during the perinatal period are likely to be effectors of these developmental changes. Because obesity is associated with an increased morbidity and mortality and because of its resistance to treatment, prevention is likely to be the best strategy for stemming the tide of the obesity epidemic. Such prevention should begin in the perinatal period with the identification and avoidance of factors which produce permanent, adverse alterations in neural pathways which control energy homeostasis.

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Metabolic Defense of the Body Weight Set Point

Cited by 26 publications

References 8 publications

Predictors of Weight Maintenance

Predictors of Weight Maintenance

Gene-Environment Interactions Controlling Energy and Glucose Homeostasis and the Developmental Origins of Obesity

Metabolic imprinting: critical impact of the perinatal environment on the regulation of energy homeostasis

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