Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of RU 486 (mitepristone), an antagonist of type II glucocorticoid receptors (GR), on the development of obesity in young 5-wk-old obese fa/fa rats has been investigated. After 15 days of treatment, body composition of obese RU 486-treated rats was similar to that of lean-vehicle rats. Analysis of body composition changes showed that RU 486 effectively reversed the obesity. It stopped fat deposition in obese rats but increased protein deposition to the level of lean-vehicle rats. RU 486 prevented the development of hyperphagia and reduced gross energetic efficiency in the obese rats but had little effect on lean rats. Brown adipose tissue mitochondrial GDP binding was increased in obese rats but was reduced in lean rats by RU 486 treatment. RU 486 also reduced the elevated activity of hippocampal glycerophosphate dehydrogenase, a glucocorticoid-responsive enzyme, of obese rats to the level of lean rats. The evidence suggests that abnormal activity of glucocorticoid GR receptors or abnormal cellular responsiveness to corticosterone receptor complexes may be important in the development of obesity in the fa/fa rat.
Am J Physiol 1990 Sep
PMID:Effects of antiglucocorticoid RU 486 on development of obesity in obese fa/fa Zucker rats. 220 81

A great deal of effort is being expended to investigate the biogenetic basis of the development and maintenance of obesity and the regulation of food intake. The task of developing and validating theoretical models of the regulation of food intake and its relationship to body weight is hampered by a lack of basic descriptive data. This study investigated the eating behavior of 96 obese women by conducting a microanalysis of 2-week baseline behavioral eating diaries. Subjects were in approximate energy balance consuming a high-fat diet (41 percent of kcal from fats) averaging 1978 kcal/day. Self-reported episodes of overeating and impulsive eating occurred frequently and were associated with situational antecedents such as eating in the car, snacking alone, friends, restaurants, availability of forbidden foods, craving sweets, tired, irritable, bored, depressed, and skipping meals. Markov chain analysis showed that overeating and impulsive eating were positively autocorrelated, suggesting the presence of an abstinence violation effect. These data suggest that eating behavior is often controlled by environmental, cognitive, and affective variables and that a complete understanding of obesity will require an integrated biobehavioral approach.
Int J Obes 1990 Sep
PMID:Obesity: a biogenetic or biobehavioral problem. 222 13

This study explored some toxicological aspects of vanadyl sulphate (VOSO4) treatment of rats made diabetic with a single intravenous injection of streptozotocin (60 mg/kg). Administered in drinking water (0.25, 0.5, 0.75 or 1 mg of VOSO4, 5H2O ml) VOSO4 treatment partially or totally corrected some of the alterations associated with the diabetic state (hyperglycaemia, polydipsia, polyphagia, high cholesterol and triglycerides levels) and did not produce any changes in various plasma or blood cell parameters which were not previously altered by diabetes. Measurement of vanadium levels indicated that tissues accumulated vanadium in the following order of concentrations: bone greater than kidney greater than spleen greater than liver greater than lung greater than or equal to muscle greater than blood. Histopathological studies did not reveal any difference in liver, stomach, ileum, spleen, heart and lung from control, non-treated diabetic or VOSO4-treated diabetic animals. Kidney of all non-treated diabetic animals showed an epithelial cellular swelling of distal tubules while only 2 of 6 VOSO4-treated diabetic animals showed this alteration. Cellular degeneration of pancreas B-cells was less marked in VOSO4-treated that in non-treated diabetic animals. The study indicates that VOSO4 may be a potential antidiabetic agent.
Pharmacol Toxicol 1990 Sep
PMID:Toxicological aspects of vanadyl sulphate on diabetic rats: effects on vanadium levels and pancreatic B-cell morphology. 225 74

Acupuncture and moxibustion is one of the important therapies in TCM for treating obese. The authors have treated 41 simple obese patients complicated with hypertension by acupuncture and moxibustion which obtained good results. In the treating group, a total effective rate was 87.8% (36 cases). For the purpose of understanding regulatory effect of acupuncture and moxibustion, the authors have observed the obesity indices, the lipid indices (TC, TG, VLDL-C, TC/HDL-C, HDL-C, LDL-C, LDL-C/HDL-C and AI), the physiological indices (saliva secretion, heart rate, respiratory rate, blood pressure and temperature) and the energy metabolism indices (BMR) in the simple obese complicated with hypertension before and after the acupuncture and moxibustion. The results showed that the therapeutic effect of acupuncture and moxibustion could have good results. At the same time, there were the benign regulatory effect of acupuncture and moxibustion in the overeating, the blood pressure, the vegetative nervous indexes, the lipid level and the energy metabolism.
Zhong Xi Yi Jie He Za Zhi 1990 Sep
PMID:[Regulatory effects of acupuncture and moxibustion on simple obese complicated with hypertension]. 226 37

The effect of estrogen supplement on selective D2 receptor antagonist sulpiride induced weight gain was examined in ovariectomized (ovx.) rats. Sulpiride injection (10 mg/kg, s.c.) showed a significant increase of body weight and food consumption only in female rats. Bilateral ovariectomy completely abolished the weight gain and hyperphagia by sulpiride. Subcutaneous injection of estradiol benzoate (E2:5 micrograms/day, s.c.) for 14 days restored the effects of sulpiride on weight gain in ovx, rats and sulpiride injection with E2 supplement significantly increased the efficiency of food utilization. The present study suggested that estrogen should be involved in the induction of overweight and hyperphagia by sulpiride.
Exp Clin Endocrinol 1990 Sep
PMID:Involvement of sex hormone in body weight gain by selective D2 receptor antagonist sulpiride. 227 23

The pharmacokinetics of oral phenobarbitone was studied in 10 clinically healthy adult dogs. The drug was given once daily in tablet form, at a dose of 5 mg kg-1 of body mass. Serial venous blood samples (n = 9) were collected from each dog on Day 1 (the first day of drug dosing), on Day 22, and on Day 24 after continuous dosing. Trough serum concentrations were determined on Day 7, Day 14 and Day 21. The drug was administered to the dogs on an empty stomach, except on Day 24, when it was given with food, in order to assess the influence of food on its absorption. Drug serum concentrations were described by a one-compartmental open model with first order absorption and elimination. An average steady-state trough serum level of phenobarbitone of 52,96 +/- 8.40 mmol l-1 was achieved after 3 weeks of daily dosing. The mean elimination half-lives for Day 1 and Day 22 were 46.3 +/- 11.3 h and 29.3 +/- 4.6 h respectively. The area under the curve for Day 22 was 1,656.17 +/- 186.45 mumol h-1 l-1 and for Day 24 was 1,493.06 +/- 205.4 mumol h-1 l-1. The mean clearance value for Day 22 was 0.0133 +/- 0.0016 l h-1 kg-1. Side effects of polyphagia, polydipsia, sedation and ataxia were commonly observed in the first 2-9 d, but disappeared thereafter. It was concluded that a dose of 5 mg kg-1 would achieve an average serum concentration of 64.59 mumol l-1 in adult dogs.(ABSTRACT TRUNCATED AT 250 WORDS)
J S Afr Vet Assoc 1990 Sep
PMID:The pharmacokinetics of phenobarbitone in fasting and non-fasting dogs. 228 6

We investigated the mechanisms of body weight regulation in young men of normal body weight leading unrestricted lives. Changes in total and resting energy expenditure, body composition, and subsequent voluntary nutrient intakes in response to overeating by 4,230 +/- 115 (SE) kJ/day (1,011 +/- 27 kcal/day) for 21 days were measured in seven subjects consuming a typical diet. On average, 85-90% of the excess energy intake was deposited (with 87% of this amount in fat and 13% in protein on average). There was no detectable difference between individuals in susceptibility to energy deposition. The resting metabolic rate, averaged for fasting and fed states, increased during overfeeding (mean +/- SE, 628 +/- 197 kJ/day, P less than 0.01), but at least some of this amount was obligatory expenditure associated with nutrient assimilation. No significant increase in energy expenditure for physical activity or thermoregulation resulted from overfeeding. Thus energy expenditure did not substantially adapt to increased energy intake. However, significant decreases in voluntary energy intake (1,991 +/- 824 kJ/day, P less than 0.05) and fat intake (48 +/- 11 g/day, P less than 0.01) followed overeating, indicating that adaptive changes in nutrient intakes can contribute significantly to body weight regulation after overeating.
Am J Physiol 1990 Sep
PMID:Energy expenditure and subsequent nutrient intakes in overfed young men. 239 4

This experiment evaluates the hypothesis that an accelerated rate of gastric emptying accounts for the hyperphagia and obesity after lesions of the ventromedial hypothalamus (VMH). Gastric emptying was measured for 16 days after the production of VMH lesions in rats maintained either ad libitum or on restricted eating. Only ad libitum VMH-lesioned rats demonstrated faster than normal rates of emptying. However, VMH rats maintained at control weights showed normal rates of gastric emptying and, even in ad libitum rats, accelerated emptying was not apparent immediately after lesions. These findings indicate that changes of emptying are not a primary effect of VMH lesions but that this dysfunction develops secondarily as a consequence of excess eating and weight gain. Measurement of stomach secretions demonstrated, however, that VMH lesions did result in an immediate and direct effect on gastric secretion. These findings mitigate the importance of gastric emptying in the etiology of the VMH syndrome. Other data consistent with this conclusion are reviewed.
Am J Physiol 1990 Sep
PMID:Accelerated gastric emptying in VMH-lesioned rats is secondary to excess weight gain. 187 9

The significance of portal venous drainage after whole-pancreas transplantation both for metabolic control and development of diabetic nephropathy was investigated. Streptozotocin-diabetic inbred LEW rats received a duct-ligated pancreas graft with either systemic or portal venous drainage and were followed for up to one year. Normal and untreated diabetic rats (n=18 in each group) served as controls. Irrespective of the route of venous drainage pancreas transplants normalized the diabetic polyuria, polyphagia, and polydipsia. Growth rates and general health did not differ from normal rats. Pancreas transplantation with portal venous drainage furthermore normalized nonfasting blood glucose and peripheral insulin levels, and intravenous glucose tolerance. Pancreas transplantation with systemic venous drainage, however, was associated with peripheral hyperinsulinemia, slightly elevated nonfasting blood glucose levels, and supranormal K-values in intravenous glucose tolerance tests. Though portal venous drainage was associated with better metabolic control than systemic venous drainage, both techniques of pancreas transplantation proved equally effective to prevent the development of diabetic glomerular membrane thickening determined 6 and 12 months posttransplant.
Transplantation 1990 Sep
PMID:Significance of portal venous drainage after whole-organ pancreas transplantation for endocrine graft function and prevention of diabetic nephropathy. 240 87

Gold thioglucose (GTG) has been known to be an obesity causing agent for over 40 years. GTG works by affecting dendrites in the mouse ventromedial hypothalamus (VMH) producing a permanent VMH lesion and subsequent hyperphagia and obesity. We have investigated the effect of beta-thioglucose (BTG), a glucose antimetabolite, on GTG-induced lesions in the VMH of mice. Twenty-eight female CF-1 mice were used in this study. Seven micron sections were made of the mouse VMH, mounted on glass slides, and stained with hematoxylin and eosin. A previous report of BTG action on GTG-induced lesions has not supported a competitive inhibition between these two drugs. Our data demonstrate that at 1/2 hour, 6 hours, and 12 hours post BTG, BTG completely inhibited GTG-induced lesions in the VMH.
Physiol Behav 1989 Sep
PMID:Beta-thioglucose inhibits gold thioglucose lesions in the ventromedial hypothalamus. 251 30


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