Corticosterone-dependent metabolic and neuroendocrine abnormalities in obese Zucker rats in relation to feeding

Duclos, Martine; Timofeeva, Elena; Michel, Chantal; Richard, Denis

doi:10.1152/ajpendo.00087.2004

Cited by 26 publications

(14 citation statements)

References 65 publications

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“…On the other hand, a lower level of circulating glucocorticoids might have contributed to the increased leptin signaling by hypothalamic neuronal networks [39] in CAP-treated rats. In fact, a reduction in glucocorticoid levels could underlie the "healthier" endocrine and metabolic profile of the CAP rats in the present study, since removal of adrenals resulting in other studies has been shown to increase insulin sensitivity and metabolism and reduce body weight gain even in rats which have a deficient leptin signaling system [40][41][42].…”

Section: Discussionmentioning

confidence: 76%

Neonatal capsaicin causes compensatory adjustments to energy homeostasis in rats

Wall

Wielinga

Strubbe

et al. 2006

Physiology & Behavior

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Several mechanisms involved in ingestive behavior and neuroendocrine activity rely on vagal afferent neuronal signaling. Seemingly contradictory to this idea are observations that vagal afferent neuronal ablation by neonatal capsaicin (CAP) treatment has relatively small effects on glucose homeostasis and long-term regulation of energy balance. It may be proposed that humoral endocrine factors and/or their sensitivities compensate for the loss of vagal afferent information, particularly when subjects face disturbances in ambient fuel levels. Therefore, male adult rats neonatally treated with CAP or with the vehicle (VEH) underwent intravenous glucose tolerance tests (IVGTTs) during which blood fuel levels, and circulating adipose, pancreatic, and adrenal hormones were assessed. CAP rats displayed similar hyperglycemia as VEH rats, but with markedly reduced plasma insulin and corticosterone responses. These results indicate that CAP rats have increased insulin sensitivity during hyperglycemic episodes, and lower plasma levels of corticosterone in CAP rats relative to VEH rats could underlie this effect. After the IVGTT, CAP rats had increased plasma adiponectin and reduced plasma resistin levels, and these alterations in adipose hormones might be relevant for post-ingestive metabolic processes. In a second experiment, anorexigenic efficacies of cholecystokinin and leptin were assessed. While VEH rats, but not CAP rats, responded with reduced food intake to i.p. injected cholecystokinin, only CAP rats responded to i.v. infused leptin with a reduction in food intake. It is concluded that reduced HPA axis activity and/or increased leptin signaling could underlie compensations in fuel handling and energy balance following CAP treatment.

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Section: Discussionmentioning

confidence: 76%

Neonatal capsaicin causes compensatory adjustments to energy homeostasis in rats

Wall

Wielinga

Strubbe

et al. 2006

Physiology & Behavior

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“…These studies showed that following 12 [65], 24 [66,67] and 48 [67] h of fasting, or following 3 weeks [64] of 33% energy restriction, there was an increase in circulating corticosterone concentrations in obese rodents. A similar effect was also seen with longer-term food deprivation.…”

Section: Effects Of Energy Restriction On Activity Of the Hpa Axis Inmentioning

confidence: 97%

Effects of energy restriction on activity of the hypothalamo-pituitary-adrenal axis in obese humans and rodents: implications for diet-induced changes in body composition

Seimon

Hostland

Silveira

et al. 2013

Hormone Molecular Biology and Clinical Investigation

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Background: Obesity treatments aim to maximize fat loss, particularly abdominal or visceral fat, without compromising lean or bone mass. However, the literature contains numerous examples of obesity treatments that -in addition to fat loss -result in loss of lean mass and/or bone mass. Materials and methods: Because of the known effects of energy restriction to increase activity of the hypothalamopitutiary adrenal (HPA) axis in lean humans and animals, and because increases in circulating glucocorticoid levels could potentially contribute to adverse body compositional changes with obesity treatments, we conducted a systematic PubMed search to determine whether HPA axis activation also occurs in response to energy restriction in obese humans and animals. Results and conclusions:In most studies in obese humans, short-term severe energy restriction increased circulating cortisol levels, and this response was also seen in two longer-term human studies involving severe or moderate energy restriction. These fi ndings parallel studies on short-or long-term energy restriction in obese rodents, with most studies showing increases in circulating corticosterone concentrations, and no change or actual increases in hypothalamic expression of corticotropin-releasing hormone, urocortin 3 or their receptors. However, a signifi cant proportion of studies involving longer-term severe or moderate energy restriction in obese humans showed no change or decreases in HPA axis function. There was variability among human studies in the duration of energy restriction and timing of the HPA axis investigations (i.e., during energy restriction, or aft er a period of post-restriction weight maintenance). In order to unambiguously determine changes in HPA axis function with energy restriction in obese humans, it will be important to assess HPA axis function at multiple time points during energy restriction, given that obese individuals may spend many

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“…Hypothalamic mRNA levels of neuropeptide Y (NPY) and proopiomelanocortin (POMC) were measured by in situ hybridization essentially as described previously (13,39). Briefly, hypothalamic sections were mounted onto poly-L-lysine-coated slides, dehydrated in ethanol, fixed in paraformaldehyde, digested with proteinase K (10 g/ml), acetylated with 0.25% acetic anhydride, and dehydrated in ethanol gradient.…”

Section: Animalsmentioning

confidence: 99%

Acute injection of ASP in the third ventricle inhibits food intake and locomotor activity in rats

Roy

Gauvreau

et al. 2011

American Journal of Physiology-Endocrinology and Metabolism

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ing protein (ASP; also known as C3adesArg) stimulates triglyceride synthesis and glucose transport via interaction with its receptor C5L2, which is expressed peripherally (adipose tissue, muscle) and centrally. Previous studies have shown that ASP-deficient mice (C3KO) and C5L2-deficient mice (C5L2KO) are hyperphagic (59 to 229% increase, P Ͻ 0.0001), which is counterbalanced by increased energy expenditure measured as oxygen consumption (V O2) and a lower RQ. The aim of the present study was to evaluate ASP's effect on food intake, energy expenditure, and neuropeptide expression. Male rats were surgically implanted with intracerebroventricular (icv) cannulas directed toward the third ventricle. After a 5-h fast, rats were injected, and food intake was assessed at 0.5, 1, 2, 4, 16, 24, and 48 h, with a 5-to 7-day washout period between each injection. Acute icv injections of ASP (0.3-1,065 pmol) had a time-dependent effect on decreasing food intake by 20 to 57% (P Ͻ 0.05). Decreases were detected by 30 min (maximum 57%, P Ͻ 0.01) and at the highest dose effects extended to 48 h (19%, P Ͻ 0.05, 24-to 48-h period). Daily body weight gain was decreased by 131% over the first 24 h and 29% over the second 24 h (P Ͻ 0.05). A conditioned taste aversion test indicated that there was no malaise. Furthermore, acute ASP injection affected energy substrate usage, demonstrated by decreased V O2 and RQ (P Ͻ 0.05; implicating greater fatty acid usage), with a 49% decrease in total activity over 24 h (P Ͻ 0.05). ASP administration also increased anorexic neuropeptide POMC expression (44%) in the arcuate nucleus, with no change in NPY. Altogether ASP may have central in addition to peripheral effects. acylation-stimulating protein; C5L2; energy metabolism; proopiomelanocortin IN RECENT YEARS, MUCH ATTENTION HAS FOCUSED on the hypothalamic-adipose axis (46). White adipose tissue (WAT), recognized originally for its capacity to store excess dietary energy in the form of triglycerides (TG), is now considered an endocrine organ because of its capacity to secrete hormones and cytokines (17). WAT is now recognized as a fundamental participant in the control of energy metabolism (22). The number of adipokines has expanded rapidly, and these include leptin, adiponectin, resistin, acylation-stimulating protein (ASP), and many more (17). The role of ASP and its involvement in the control of energy balance and in the development of obesity have been actively studied in our group for the last decade.ASP promotes TG synthesis in WAT through interaction with its cell surface receptor C5L2. Activation and phosphorylation of C5L2 leads to increased fatty acid uptake, increased glucose transport, and stimulation of diacylglycerol acyltransferase activity (9,10,19,20). ASP is produced through cleavage of the precursor protein complement C3 via factor B and adipsin (factor D) interaction generating C3a, which is rapidly desarginated to produce ASP (also known as C3adesArg) (6, 25). C3-knockout mice (C3 Ϫ/Ϫ ; also known as C3KO) are deficient in AS...

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Corticosterone-dependent metabolic and neuroendocrine abnormalities in obese Zucker rats in relation to feeding

Cited by 26 publications

References 65 publications

Neonatal capsaicin causes compensatory adjustments to energy homeostasis in rats

Neonatal capsaicin causes compensatory adjustments to energy homeostasis in rats

Effects of energy restriction on activity of the hypothalamo-pituitary-adrenal axis in obese humans and rodents: implications for diet-induced changes in body composition

Acute injection of ASP in the third ventricle inhibits food intake and locomotor activity in rats

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