Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0038187 (starvation)
 24,951 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of glucocorticoid (GC) on the enzyme overshoot response to starvation-refeeding (S-R) and on tritium incorporation into lipids was studied. Long-term effects of hypercortisolism on carcass and liver lipids were also determined. In the first series of experiments, intact, adrenalectomized (ADX) and ADX, GC-replaced rats were either ad libitum fed or starved and refed a 65% glucose diet. Glucose-6-phosphate dehydrogenase and malic enzyme activities in both liver and adipose tissue were determined as were the liver and fat pad lipid levels, hepatic and muscle glycogen content, and in vivo incorporation of 3H (from 3HOH, 1 mCi/100 g b.w.) into liver, adipose tissue and plasma lipids. The role for GC in the enzyme overshoot in S-R rats was reaffirmed as was the effect of ADX on enzyme activity and adipose tissue lipid. Hepatic glycogen content was reduced by adrenalectomy and not reversed by GC replacement in the ad libitum-fed animals. S-R reduced liver glycogen in the intact rats, did not affect liver glycogen in ADX-GC replaced rats and increased liver glycogen in the untreated ADX animals. S-R increased hepatic and adipose tissue lipid synthesis as measured by 3H incorporation. This effect was reduced by ADX and the ADX effect was reversed by GC. Prolonged administration of GC had no effect on increasing hepatic or carcass lipid content of ad libitum-fed animals. Results of these experiments suggest that while ineffective in inducing lipogenesis in ad libitum-fed animals, GC plays a role in the lipogenic response to starvation-refeeding and that this effect is apart from its role in the induction of the enzyme overshoot.
 ...
PMID:Role of glucocorticoid in adaptive hyperlipogenesis in the rat. 735

Natural or experimental starvation is frequently associated with hypercortisolism, reflected as incomplete suppression of serum cortisol after dexamethasone. To determine whether rapid weight loss per se or some other aspect of starvation induces disruption of the hypothalamic-pituitary-adrenal (HPA) axis, we evaluated 2 categories of obese women (body mass index > 30 kg/m2) undergoing rapid weight loss: binge eaters (n = 12) and nonbinge eaters (n = 8). We performed psychometric evaluation and 1 mg overnight dexamethasone suppression tests in the obese subjects, as well as in 12 race- and age-matched normal-weight women. The obese women were tested before and after 12 weeks of a 3349 kJ/day (800 kcal/day) liquid formula diet, and lost an average of 19.3 kg, which represented 17.3% of their total body weight. Binge eaters, who were initially more depressed than either nonbinge eaters or normal-weight controls, had a significant amelioration of their symptoms with weight loss. Neither group had evidence of disruption of the HPA axis before or after weight loss. Thus, the rate of failure to suppress cortisol after dexamethasone was approximately 10% in each of the obese and control groups, and did not differ between the pre- and postweight loss condition or between binge eaters and nonbinge eaters. Serum free T4 was unchanged, whereas T3 fell significantly with weight loss. We conclude that weight loss may improve affect in the obese without altering HPA axis activity, and postulate that one of the concomitants of restricted energy intake, perhaps in combination with a threshold body weight, may be of greater importance in causing abnormalities of dexamethasone suppression testing than rapid weight loss per se.
 ...
PMID:Normal dexamethasone suppression in obese binge and nonbinge eaters with rapid weight loss. 844 25

In the rat, high-dose corticosterone (Cort) administration, the hypercortisolism of starvation, and adrenalectomy are all associated with decreased food intake and weight loss. We report here a study of the effects of high-dose Cort administration, starvation, and adrenalectomy on two peripheral hormones known to influence food intake and energy use, insulin and leptin. We also studied the impact of these interventions on the levels of type 2 corticotropin-releasing hormone receptor (CRHR-2) mRNA in the hypothalamic paraventricular nucleus (PVN) and ventromedial hypothalamus (VMH). The VMH is classically referred to as the satiety center because electrical stimulation of the VMH leads to inhibition of food intake, whereas CRHR-2 are thought to transduce the profound anorexogenic effects of CRH or its related peptide urocortin. Starvation and adrenalectomy each lowered plasma insulin and leptin levels and were associated with decrements in CRHR-2 mRNA levels in the VMH. Cort administration increased plasma leptin levels profoundly, as well as plasma insulin levels and the levels of VMH CRHR-2 mRNA. Under all experimental conditions, a positive correlation was seen between plasma leptin levels and VMH CRHR-2 mRNA. These data suggest that decreased food intake and weight loss after high-dose Cort administration at least partially depend on the profound impact of Cort on plasma leptin secretion in the rat; they suggest, moreover, an additional mechanism for the satiety-inducing effects of leptin, namely increasing CRHR-2 in the VMH. The concordance of a fall in plasma insulin and leptin levels with the fall in VMH CRHR-2 mRNA levels further supports the idea that compensatory responses during starvation and adrenalectomy include not only the disinhibiting effects of reduced insulin and leptin levels on appetite through already-described mechanisms but also via an effect of leptin on VMH CRHR-2. Neither Cort administration, starvation, nor adrenalectomy influenced the levels of CRHR-2 mRNA in the PVN, suggesting that these receptors are differentially regulated in different hypothalamic regions.
 ...
PMID:Altered expression of type 2 CRH receptor mRNA in the VMH by glucocorticoids and starvation. 975 44

Numerous endocrine abnormalities are associated with anorexia nervosa and bulimia nervosa. The principal complication is amenorrhoea. Hypothyroidism and hypercortisolism have been described as a protective mechanism to conserve energy. Growth hormone concentrations are often increased as a result of starvation. Insulin and blood sugar concentrations are decreased, but prolactin concentrations are remain normal. Considerable evidence exists of hypothalamic dysfunction in patients with eating disorders. This dysfunction is reflected in disturbances of endocrine function. Endocrine disturbances may be not solely related to the low body weight. Hypothalamic monoamines, neuropeptides and leptin are involved in the regulation of human appetite, and in several ways they are changed in eating disorders. However, it remains to be clarified whether the altered appetite regulation is secondary or etiologic.
 ...
PMID:[Endocrine and reproductive disturbances in anorexia nervosa and bulimia nervosa]. 1126 7

Corticotropin-releasing hormone (CRH) is one of the anorexigenic neuropeptides, and indeed the expression of hypothalamic CRH is known to be inhibited by starvation. To clarify whether elevated plasma glucocorticoid during starvation is responsible for the CRH suppression, we examined the expression level of hypothalamic CRH mRNA after food deprivation in adrenalectomized, plasma corticosterone (B)-clamped animals. Male Wistar rats were divided into 2 groups: one group had adrenalectomy (ADX) and B pellet implantation (ADX+B, n=42), and the other group had only sham operation (sham, n=42). Rats were then treated with either ad libitum food supply or food deprivation for up to 96 h. The expression of CRH mRNA in the paraventricular nucleus (PVN) was estimated by in situ hybridization. After food deprivation, mean plasma B level was markedly elevated in sham group, but almost clamped in the ADX+B group. In this experimental condition, CRH mRNA in the PVN was significantly decreased in the sham group, whereas no change was obtained in the ADX+B group. Our data suggest the decrease in CRH mRNA seems to be related to the elevated glucocorticoid level during starvation. The status of hyperadrenocorticism without activation of CRH led us to speculate that adrenocortical function is predominant in the hypothalamic-pituitary-adrenal (HPA) axis during starvation.
 ...
PMID:CRH mRNA expression in the hypothalamic paraventricular nucleus is inhibited despite the activation of the hypothalamo-pituitary-adrenal axis during starvation. 1861 22