Decreased food intake following overfeeding involves leptin-dependent and leptin-independent mechanisms

White, Christy L.; Purpera, Megan N.; Ballard, Kenny; Morrison, Christopher D.

doi:10.1016/j.physbeh.2010.04.006

Cited by 32 publications

(43 citation statements)

References 40 publications

(29 reference statements)

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“…Recently, using leptin receptor-deficient obese Zucker (fa/ fa) rats, White et al [14] demonstrated that intact leptin signaling is not required for the decrease in food intake that occurs during overfeeding. Evidently, more studies are needed to determine whether leptin is involved in the mechanism for food intake reduction during HFD feeding.…”

Section: Discussionmentioning

confidence: 99%

Leptin resistance does not induce hyperphagia in the rat

et al. 2011

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Leptin has been thought to work as a mediator for body weight control by inhibiting food intake. Leptin, however, cannot prevent obesity induced by a high-fat diet (HFD) probably because of leptin resistance. We investigated daily feeding and weight gain when ordinary chow (OC) was changed to a HFD in male rats. Food intake, by weight, significantly increased the next day, but gradually decreased until at 20 days the HFD intake contained the same calories as consumed by the OC-fed control rats. The reduction in food intake occurred only during the night without change of preference for the HFD, even after leptin resistance had developed. Nonetheless, the HFD-fed rats gained more weight than the controls. From the present experiment, it is concluded that leptin resistance does not induce hyperphagia, and suggested that body weight is not regulated to be constant.

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Section: Discussionmentioning

confidence: 99%

Leptin resistance does not induce hyperphagia in the rat

et al. 2011

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“…However, brief periods of excess or reduced energy intake often succeed one another. Intermittent periods of OF (e.g., holiday weight gain) are often compensated by subsequent self-imposed CR, 22,23 whereas periods of CR are likely to be followed by excessive energy intake (e.g., yo-yo dieting). 23,24 Thus, the purpose of the present study was an intra-individual comparison of the effects of consecutive, controlled 1-week periods of altered energy balance (i.e., CR followed by RF, and OF followed by CR) on IS and insulin secretion in a group of healthy lean men.…”

Section: Introductionmentioning

confidence: 99%

Effects of brief perturbations in energy balance on indices of glucose homeostasis in healthy lean men

et al. 2011

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BACKGROUND:Little is known about the effects of short-term caloric restriction (CR) and overfeeding (OF) on glucose homeostasis in healthy lean individuals. In addition, it remains unclear whether the effects of CR and OF are reversed by a complementary feeding period. METHODS: Ten healthy men participated in two cycles of controlled 7-day periods of CR and refeeding (RF; protocol A), and OF and CR (protocol B) at ±60% energy requirement. At baseline, insulin sensitivity (IS) was assessed by euglycemic clamp (M). Before and during each feeding cycle, fasting and oral glucose tolerance test-derived indices were used to estimate glucose tolerance, IS and glucose-stimulated insulin secretion. RESULTS: Clamp tests revealed normal IS at baseline (M-values 9.4 ± 2.1 mg kg À1 min À1 , coefficient of variation (CV) inter 22%). M-values were significantly correlated with indices of IS. In protocol A, CR-induced weight loss (À3.0±0.4 kg) was associated with an increase in fasting IS. Postprandial IS and glucose-stimulated insulin secretion remained unchanged, but glucose tolerance decreased. RF decreased fasting and postprandial IS at increased glucose-stimulated insulin secretion. In protocol B, OF significantly increased the body weight ( þ 1.6±0.9 kg). Concomitantly, fasting and postprandial IS decreased at increased glucose-stimulated insulin secretion. Subsequent CR reversed these effects. Inter-individual variability in indices of glucose metabolism was high with coefficients of variation ranging from 9 to 59%. CONCLUSION: Significant changes in glucose metabolism are evident within 7-day periods of controlled OF and underfeeding. Although IS was impaired at the end of the CR --RF cycle, IS was normalized after the OF --CR cycle. At different feeding regimens, homeostatic responses of glucose metabolism were highly variable. Keywords: insulin secretion; insulin sensitivity; glucose homeostasis; weight gain; energy balance INTRODUCTION Long-term perturbations in energy balance, either by overfeeding (OF) or underfeeding, are known to modulate insulin sensitivity (IS). Chronic OF and obesity are commonly characterized by insulin resistance, 1 which has been shown to be completely 2 or partially reversed by acute caloric restriction (CR), as well as by moderate weight loss. 3 --5 On the other hand, IS is preserved or even improved with chronic CR in patients with anorexia nervosa and returned to normal values at the end of refeeding (RF). 6 Although considerable research has been devoted to individuals outside the normal range of body weight, there are only few studies examining the effects of short-term controlled perturbations in energy balance on IS in lean subjects without confounding metabolic abnormalities. 7 --17 Moreover, these studies provide discordant findings that may depend on duration and degree of energy imbalance and macronutrient composition of the diets. Fasting (1 --3 days) consistently caused a decline in IS assessed by clamp-and intravenous glucose tolerance test. 7,8,17 Studies with less severe ...

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“…Defense of a certain body weight can be ascertained by observing the metabolic and behavioral reactions to experimental perturbations usually accomplished by transient over-or underfeeding. 7,8 In our rat model of RYGB, 9,10 we have used chronic intracerebroventricular infusion of the melanocortin receptor antagonist SHU9119 to stimulate food intake. 11 As shown earlier, 12 SHU9119 powerfully stimulates food intake and over a 2-week infusion period results in significant weight gain and obesity in normal, chow fed as well as high-fat fed rats, 11 reminiscent of rats and mice with MC4R deficiency.…”

Section: Behavioral Evidence For Rygb-induced Change In Defended Bodymentioning

confidence: 99%

“…11 When infusion was stopped, they returned to the same low body weight before infusion, clearly demonstrating that this low body weight is actively defended and not the result of an imposed physical restriction. We preferred this approach over forced intragastric feeding that results in the same voluntary feeding suppression 7,8 because it is more powerful and less invasive. Consistent with our findings, transient hyperphagia and weight gain was also observed in female rats with sleeve gastrectomy during pregnancy and lactation.…”

Section: Behavioral Evidence For Rygb-induced Change In Defended Bodymentioning

confidence: 99%

“…Although this factor is distinct from leptin, it requires intact leptin signaling, as shown by the absence of food intake suppression following a period of intragastric overnutrition in leptin receptor-deficient Zucker rats. 8 Although normal rats intragastrically 'overfed' for 10 days progressively suppress voluntary food intake and exhibit complete anorexia for a few days following cessation of infusion, Zucker rats immediately return to pre-infusion food intake upon cessation. 8 It is thus possible that this factor has a role in the suppression of food intake and increase of energy expenditure after RYGB.…”

Section: Potential Underlying Mechanisms For Change In Set Pointmentioning

confidence: 99%

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Does gastric bypass surgery change body weight set point?

et al. 2016

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The relatively stable body weight during adulthood is attributed to a homeostatic regulatory mechanism residing in the brain which uses feedback from the body to control energy intake and expenditure. This mechanism guarantees that if perturbed up or down by design, body weight will return to pre-perturbation levels, defined as the defended level or set point. The fact that weight re-gain is common after dieting suggests that obese subjects defend a higher level of body weight. Thus, the set point for body weight is flexible and likely determined by the complex interaction of genetic, epigenetic and environmental factors. Unlike dieting, bariatric surgery does a much better job in producing sustained suppression of food intake and body weight, and an intensive search for the underlying mechanisms has started. Although one explanation for this lasting effect of particularly Roux-en-Y gastric bypass surgery (RYGB) is simple physical restriction due to the invasive surgery, a more exciting explanation is that the surgery physiologically reprograms the body weight defense mechanism. In this non-systematic review, we present behavioral evidence from our own and other studies that defended body weight is lowered after RYGB and sleeve gastrectomy. After these surgeries, rodents return to their preferred lower body weight if over-or underfed for a period of time, and the ability to drastically increase food intake during the anabolic phase strongly argues against the physical restriction hypothesis. However, the underlying mechanisms remain obscure. Although the mechanism involves central leptin and melanocortin signaling pathways, other peripheral signals such as gut hormones and their neural effector pathways likely contribute. Future research using both targeted and non-targeted 'omics' techniques in both humans and rodents as well as modern, genetically targeted, neuronal manipulation techniques in rodents will be necessary.

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Decreased food intake following overfeeding involves leptin-dependent and leptin-independent mechanisms

Cited by 32 publications

References 40 publications

Leptin resistance does not induce hyperphagia in the rat

Leptin resistance does not induce hyperphagia in the rat

Effects of brief perturbations in energy balance on indices of glucose homeostasis in healthy lean men

Does gastric bypass surgery change body weight set point?

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