Glucocorticoids reverse leptin effects on food intake and body fat in mice without increasing NPY mRNA

1999 ◽  
Vol 277 (4) ◽  
pp. E708-E716 ◽  
Author(s):  
Joel M. Solano ◽  
Lauren Jacobson
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Body Fat ◽  
Mrna Levels ◽  
Plasma Insulin Levels ◽  
Significant Attenuation ◽  
Induced Changes ◽  
Leptin Expression ◽  
Stimulation Of

Glucocorticoid stimulation of appetite and leptin expression conflicts with leptin inhibition of food intake and suggests that glucocorticoids reduce sensitivity to leptin. To determine if glucocorticoids impair feeding and metabolic responses to leptin, we measured leptin-induced changes in food intake, body weight, hormones, carcass fat, and hypothalamic neuropeptide Y (NPY) mRNA in adrenalectomized mice with and without corticosterone replacement. Leptin infusion (0.5 μg/h) significantly decreased food intake and body weight in adrenalectomized mice. Corticosterone replacement approximating normal 24-h mean levels restored food intake but did not permit weight gain equivalent to PBS-infused controls. Corticosterone levels comparable to stress-induced production completely reversed leptin-induced reductions in weight gain and body fat, despite significant attenuation by leptin of corticosterone-induced increases in plasma insulin levels. Glucocorticoid replacement increased food intake without reversing leptin inhibition of hypothalamic NPY mRNA levels. We conclude that glucocorticoid levels within the physiological range can interfere with leptin action and that glucocorticoid effects are at least partly independent of NPY.

Effect of intracerebroventricular α-MSH on food intake, adiposity, c-Fos induction, and neuropeptide expression

2000 ◽  
Vol 279 (2) ◽  
pp. R695-R703 ◽  
Author(s):  
Julie E. McMinn ◽  
Charles W. Wilkinson ◽  
Peter J. Havel ◽  
Stephen C. Woods ◽  
Michael W. Schwartz
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Energy Homeostasis ◽  
Melanocortin Receptor ◽  
Mrna Levels ◽  
Melanocyte Stimulating Hormone ◽  
The Third ◽  
Chronic Infusion ◽  
Plasma Insulin Levels ◽  
Cumulative Food Intake

α-Melanocyte-stimulating hormone (α-MSH) is a hypothalamic neuropeptide proposed to play a key role in energy homeostasis. To investigate the behavioral, metabolic, and hypothalamic responses to chronic central α-MSH administration, α-MSH was infused continuously into the third cerebral ventricle of rats for 6 days. Chronic α-MSH infusion reduced cumulative food intake by 10.7% ( P < 0.05 vs. saline) and body weight by 4.3% ( P < 0.01 vs. saline), which in turn lowered plasma insulin levels by 29.3% ( P < 0.05 vs. saline). However, α-MSH did not cause adipose-specific wasting nor did it alter hypothalamic neuropeptide mRNA levels. Central α-MSH infusion acutely activated neurons in forebrain areas such as the hypothalamic paraventricular nucleus, as measured by a 254% increase in c-Fos-like immunoreactivity ( P < 0.01 vs. saline), as well as satiety pathways in the hindbrain. Our findings suggest that, although an increase of central melanocortin receptor signaling acutely reduces food intake and body weight, its anorectic potency wanes during chronic infusion and causes only a modest decrease of body weight.

scholarly journals Impaired Leptin Expression and Abnormal Response to Fasting in Corticotropin-Releasing Hormone-Deficient Mice

Endocrinology ◽  
2004 ◽  
Vol 145 (7) ◽  
pp. 3174-3181 ◽  
Author(s):  
Kyeong-Hoon Jeong ◽  
Satoru Sakihara ◽  
Eric P. Widmaier ◽  
Joseph A. Majzoub
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Energy Storage ◽  
Food Intake ◽  
Physiological Role ◽  
Natural Conditions ◽  
Abnormal Response ◽  
Abnormal Increase ◽  
Leptin Expression ◽  
Deficient Mice

Abstract Leptin has been postulated to comprise part of an adipostat, whereby during states of excessive energy storage, elevated levels of the hormone prevent further weight gain by inhibiting appetite. A physiological role for leptin in this regard remains unclear because the presence of excessive food, and therefore the need to restrain overeating under natural conditions, is doubtful. We have previously shown that CRH-deficient (Crh−/−) mice have glucocorticoid insufficiency and lack the fasting-induced increase in glucocorticoid, a hormone important in stimulating leptin synthesis and secretion. We hypothesized that these mice might have low circulating leptin. Indeed, Crh−/− mice exhibited no diurnal variation of leptin, whereas normal littermates showed a clear rhythm, and their leptin levels were lower than their counterparts. A continuous peripheral CRH infusion to Crh−/− mice not only restored corticosterone levels, but it also increased leptin expression to normal. Surprisingly, 36 h of fasting elevated leptin levels in Crh−/− mice, rather than falling as in normal mice. This abnormal leptin change during fasting in Crh−/− mice was corrected by corticosterone replacement. Furthermore, Crh−/− mice lost less body weight during 24 h of fasting and ate less food during refeeding than normal littermates. Taken together, we conclude that glucocorticoid insufficiency in Crh−/− mice results in impaired leptin production as well as an abnormal increase in leptin during fasting, and propose that the fast-induced physiological reduction in leptin may play an important role to stimulate food intake during the recovery from fasting.

Loss of body fat in lean parabiotic partners of ob/ob mice

1997 ◽  
Vol 272 (6) ◽  
pp. R1809-R1815 ◽  
Author(s):  
R. B. Harris
Keyword(s):  
Food Intake ◽  
Mrna Expression ◽  
Body Fat ◽  
Rectal Temperature ◽  
Serum Insulin ◽  
Serum Leptin ◽  
Leptin Expression

The objective of this experiment was to confirm whether changes in serum leptin and leptin expression were consistent with it being the "lipostatic" factor implicated by earlier parabiosis studies. Lean (+/?) and obese (ob/ob) female C57B1/6J-ob mice were parabiosed (lean-ob/ob) at 7 wk of age. Controls were ob/ob-ob/ob and lean-lean pairs, and single lean and ob/ob mice. Pairs were maintained for 50 days. In ob/ob members of lean-ob/ob pairs serum insulin was normalized, food intake was suppressed, and body fat was reduced by 14%. Lean partners of ob/ob mice had a reduced rectal temperature and experienced a 37% reduction in body fat. Despite loss of fat, serum leptin and adipose leptin mRNA expression were unchanged in lean partners of ob/ob mice. These results suggest that, in lean-ob/ob parabiotic pairs, the ob/ob mouse responds to leptin originating in the lean parabiont, whereas the lean partner responds to a circulating signal, originating in the ob/ob mouse, that maintains leptin expression at inappropriate levels for the degree of adiposity of the lean animal.

scholarly journals Neonatal nutritional programming impairs adiponectin effects on energy homeostasis in adult life of male rats

2018 ◽  
Vol 315 (1) ◽  
pp. E29-E37 ◽  
Author(s):  
Mariana Peduti Halah ◽  
Paula Beatriz Marangon ◽  
Jose Antunes-Rodrigues ◽  
Lucila L. K. Elias
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Food Intake ◽  
White Adipose Tissue ◽  
Energy Homeostasis ◽  
Body Weight Gain ◽  
Adult Life ◽  
Male Rats ◽  
Nutritional Programming

Neonatal nutritional changes induce long-lasting effects on energy homeostasis. Adiponectin influences food intake and body weight. The aim of this study was to investigate the effects of neonatal nutritional programming on the central stimulation of adiponectin. Male Wistar rats were divided on postnatal (PN) day 3 in litters of 3 (small litter, SL), 10 (normal litter, NL), or 16 pups/dam (large litter, LL). We assessed body weight gain for 60 days, adiponectin concentration, and white adipose tissue weight. We examined the response of SL, NL, and LL rats on body weight gain, food intake, oxygen consumption (V̇o2), respiratory exchange ratio (RER), calorimetry, locomotor activity, phosphorylated-AMP-activated protein kinase (AMPK) expression in the hypothalamus, and uncoupling protein (UCP)-1 in the brown adipose tissue after central stimulus with adiponectin. After weaning, SL rats maintained higher body weight gain despite similar food intake compared with NL rats. LL rats showed lower body weight at weaning, with a catch up afterward and higher food intake. Both LL and SL groups had decreased plasma concentrations of adiponectin at PN60. SL rats had increased white adipose tissue. Central injection of adiponectin decreased body weight and food intake and increased V̇o2, RER, calorimetry, p-AMPK and UCP- 1 expression in NL rats, but it had no effect on SL and LL rats, compared with the respective vehicle groups. In conclusion, neonatal under- and overfeeding induced an increase in body weight gain in juvenile and early adult life. Unresponsiveness to central effects of adiponectin contributes to the imbalance of the energy homeostasis in adult life induced by neonatal nutritional programming.

Protein appetite is increased after central leptin-induced fat depletion

2007 ◽  
Vol 293 (4) ◽  
pp. R1468-R1473 ◽  
Author(s):  
Michael F. Wiater ◽  
Bryan D. Hudson ◽  
Yvette Virgin ◽  
Sue Ritter
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Body Fat ◽  
Caloric Intake ◽  
Sprague Dawley ◽  
Body Protein ◽  
Macronutrient Selection ◽  
Daily Diet ◽  
Nadir Point ◽  
And Control

Leptin reduces body fat selectively, sparing body protein. Accordingly, during chronic leptin administration, food intake is suppressed, and body weight is reduced until body fat is depleted. Body weight then stabilizes at this fat-depleted nadir, while food intake returns to normal caloric levels, presumably in defense of energy and nutritional homeostasis. This model of leptin treatment offers the opportunity to examine controls of food intake that are independent of leptin's actions, and provides a window for examining the nature of feeding controls in a “fatless” animal. Here we evaluate macronutrient selection during this fat-depleted phase of leptin treatment. Adult, male Sprague-Dawley rats were maintained on standard pelleted rodent chow and given daily lateral ventricular injections of leptin or vehicle solution until body weight reached the nadir point and food intake returned to normal levels. Injections were then continued for 8 days, during which rats self-selected their daily diet from separate sources of carbohydrate, protein, and fat. Macronutrient choice differed profoundly in leptin and control rats. Leptin rats exhibited a dramatic increase in protein intake, whereas controls exhibited a strong carbohydrate preference. Fat intake did not differ between groups at any time during the 8-day test. Despite these dramatic differences in macronutrient selection, total daily caloric intake did not differ between groups except on day 2. Thus controls of food intake related to ongoing metabolic and nutritional requirements may supersede the negative feedback signals related to body fat stores.

A comparison of the effects of infection with Eimeria maxima and dietary restriction on weight gain, plasma metabolites and liver glycogen in the immature fowl, Gallus domesticus

Parasitology ◽  
1982 ◽  
Vol 84 (2) ◽  
pp. 205-213 ◽  
Author(s):  
H. D. Chapman ◽  
D. L. Fernandes ◽  
T. F. Davison
Keyword(s):  
Growth Rate ◽  
Body Weight ◽  
Uric Acid ◽  
Weight Gain ◽  
Food Intake ◽  
Acute Phase ◽  
Plasma Glucose ◽  
Liver Glycogen ◽  
Plasma Metabolites ◽  
Eimeria Maxima

SUMMARYThe effects of Eimeria maxima or restricted pair-feeding on weight gain, plasma concentrations of protein, glucose, free fatty acids (FFA) and uric acid and liver glycogen were compared in immature fowl. Food intake/kg body weight and weight gain decreased during the acute phase of infection (days 5–7) while weight loss was prolonged for an extra day compared with pair-fed birds. During recovery, food intake/kg body weight of infected birds was greater than that of non-infected controls but there was no evidence for an increase in growth rate compared with controls when body weight was considered. Growth rate of pair-fed birds was greater than that of infected birds during recovery, indicating their better use of ingested food. Liver glycogen and plasma protein concentration were decreased during the acute phase of infection but the concentrations of plasma glucose, free fatty acid (FFA) and uric acid were not affected. In pair-fed birds liver glycogen was depleted, concentrations of plasma glucose and uric acid decreased and FFA increased, and these changes persisted for the remainder of the experiment. The findings are similar to those in birds whose food has been withheld and were probably due to the pattern of food intake imposed by the experimental protocol. It is concluded that the metabolic differences between infected and pair-fed birds are of doubtful significance.

Influence of Dietary Fat and Carbohydrate on Food Intake, Body Weight and Body Fat of Adult Dogs

1978 ◽  
Vol 157 (2) ◽  
pp. 278-281 ◽  
Author(s):  
D. R. Romsos ◽  
M. J. Hornshuh ◽  
G. A. Leveille
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Body Fat ◽  
Dietary Fat

scholarly journals The Gut Microbiome Derived From Anorexia Nervosa Patients Impairs Weight Gain and Behavioral Performance in Female Mice

Endocrinology ◽  
2019 ◽  
Vol 160 (10) ◽  
pp. 2441-2452 ◽  
Author(s):  
Tomokazu Hata ◽  
Noriyuki Miyata ◽  
Shu Takakura ◽  
Kazufumi Yoshihara ◽  
Yasunari Asano ◽  
...  
Keyword(s):  
Body Weight ◽  
Anorexia Nervosa ◽  
Weight Gain ◽  
Food Intake ◽  
Brain Stem ◽  
Body Weight Gain ◽  
Field Tests ◽  
Compulsive Behavior ◽  
The Brain ◽  
Poor Weight Gain

Abstract Anorexia nervosa (AN) results in gut dysbiosis, but whether the dysbiosis contributes to AN-specific pathologies such as poor weight gain and neuropsychiatric abnormalities remains unclear. To address this, germ-free mice were reconstituted with the microbiota of four patients with restricting-type AN (gAN mice) and four healthy control individuals (gHC mice). The effects of gut microbes on weight gain and behavioral characteristics were examined. Fecal microbial profiles in recipient gnotobiotic mice were clustered with those of the human donors. Compared with gHC mice, gAN mice showed a decrease in body weight gain, concomitant with reduced food intake. Food efficiency ratio (body weight gain/food intake) was also significantly lower in gAN mice than in gHC mice, suggesting that decreased appetite as well as the capacity to convert ingested food to unit of body substance may contribute to poor weight gain. Both anxiety-related behavior measured by open-field tests and compulsive behavior measured by a marble-burying test were increased only in gAN mice but not in gHC mice. Serotonin levels in the brain stem of gAN mice were lower than those in the brain stem of gHC mice. Moreover, the genus Bacteroides showed the highest correlation with the number of buried marbles among all genera identified. Administration of Bacteroides vulgatus reversed compulsive behavior but failed to exert any substantial effect on body weight. Collectively, these results indicate that AN-specific dysbiosis may contribute to both poor weight gain and mental disorders in patients with AN.

Modest weight gain is associated with sympathetic neural activation in nonobese humans

2007 ◽  
Vol 292 (5) ◽  
pp. R1834-R1838 ◽  
Author(s):  
Christopher L. Gentile ◽  
Jeb S. Orr ◽  
Brenda M. Davy ◽  
Kevin P. Davy
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Weight Gain ◽  
Body Fat ◽  
Muscle Sympathetic Nerve Activity ◽  
Fat Distribution ◽  
Abdominal Fat ◽  
Neural Activation ◽  
Burst Frequency ◽  
Weight Stability

We tested the hypothesis that modest, overfeeding-induced weight gain would increase sympathetic neural activity in nonobese humans. Twelve healthy males (23 ± 2 years; body mass index, 23.8 ± 0.7) were overfed ∼1,000 kcal/day until a 5-kg weight gain was achieved. Muscle sympathetic nerve activity (MSNA, microneurography), blood pressure, body composition (dual energy X-ray absorptiometry), and abdominal fat distribution (computed tomography) were measured at baseline and following 4 wk of weight stability at each individual's elevated body weight. Overfeeding increased body weight (73.5 ± 3.1 vs. 78.4 ± 3.2 kg, P < 0.001) and body fat (14.9 ± 1.2 vs. 18 ± 1.1 kg, P < 0.001) in 42 ± 8 days. Total abdominal fat increased (220 ± 22 vs. 266 ± 22 cm2, P < 0.001) with weight gain, due to increases in both subcutaneous (158 ± 15 vs. 187 ± 12 cm2, P < 0.001) and visceral fat (63 ± 8 vs. 79 ± 12 cm2, P = 0.004). As hypothesized, weight gain elicited increases in MSNA burst frequency (32 ± 2 vs. 38 ± 2 burst/min, P = 0.002) and burst incidence (52 ± 4 vs. 59 ± 3 bursts/100 heart beats, P = 0.026). Systolic, but not diastolic blood pressure increased significantly with weight gain. The change in MSNA burst frequency was correlated with the percent increase in body weight ( r = 0.59, P = 0.022), change in body fat ( r = 0.52, P = 0.043) and percent change in body fat ( r = 0.51, P = 0.045). The results of the current study indicate that modest diet-induced weight gain elicits sympathetic neural activation in nonobese males. These findings may have important implications for understanding the link between obesity and hypertension.

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