Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a nationwide survey the nutritional status was assessed of 539 apparently healthy, independently living elderly aged 65-79 years. Anthropometric data showed no energy deficits. The prevalence of anemia was 4 and 1% among men and women, respectively. Many elderly showed a low level of 25-hydroxyvitamin D in plasma (less than 31 nmol/L: men 35%; women 43%), indicating a marginal status. Although the prevalence of low blood levels of folate, pyridoxal-5'-phosphate, and total carotenoids was higher among the elderly than among younger adults, clear (clinical) signs of nutritional deficiencies were not observed. Prevalence of obesity (13%), hypercholesterolemia (38%), and hypertension (63%) was found to be high, the percentages being higher for women than for men. Several indicators of the nutritional status appeared to differ among age groups. It is concluded that few differences can be considered as being due to physiological aging, which finding should be reflected in reference values for elderly people.
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PMID:Nutrition and aging: nutritional status of "apparently healthy" elderly (Dutch nutrition surveillance system). 230 4

Obesity due to overfeeding in one parabiotic rat results in mild hypophagia and specific loss of fat from its partner. Studies were conducted to determine whether the changes in body composition were reversible and whether the nonsignificant reduction in food intake was a primary response to a humoral lipostatic factor. Tube feeding partners of overfed rats 0.5 g more food per day than eaten voluntarily prevented loss of fat, although hepatic and adipose glucose-6-phosphate dehydrogenase activities were depressed. Glucose flux through the pentose phosphate pathway was inhibited in both adipose and hepatic tissue from thin partners of obese rats, although fatty acid synthesis was depressed only in adipose tissue. Response to insulin by adipocytes from ad libitum partners of obese rats appeared to be blunted, but insulin sensitivity was normal. When overfeeding stopped, both partners returned to control body composition, suggesting that the changes observed in parabiotic partners of obese rats were physiological responses to a putative circulating lipostatic factor rather than a nonspecific consequence of parabiosis.
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PMID:Site of action of putative lipostatic factor: food intake and peripheral pentose shunt activity. 237 28

A total of 111 patients with essential hypertension (the II stage) and obesity (the II degree) were investigated for providing with vitamin B6. The functional methods used for the vitamin assay (ACT activity of red blood cells and pyrodoxale-5-phosphate effect) have revealed significant vitamin B6 deficiency in 81.1% of the patients. Vitamin B6 deficiency was intensified in the course of the dietotherapy. Correction of vitamin B6 deficiency with a therapeutic dose of pyridoxine (20 mg/day) during 20-22 days, in the presence of the diet, has promoted optimization of providing with vitamin B6: normalization of pyrodoxale-5-phosphate effect. The hypotensive effect and decrease of excessive body mass in patients who received dietotherapy and pyridoxine (20 mg/day) were more pronounced than in those who received the same diet and the multivitamin "Undevitum".
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PMID:[The vitamin B6 allowance of hypertension patients and the effect of dietotherapy]. 239 75

We evaluated the effects of phenobarbital, an inducer, on plasma glucose and serum immunoreactive insulin levels and on hepatic glucose and drug metabolism using an animal model of non-insulin dependent diabetes mellitus. Genetically obese (ob/ob) mice, characterized by hyperglycaemia, hyperinsulinaemia, fatty liver and obesity were selected. The impairment of diabetic state with age was associated with increased activities of NADPH producing enzymes, whereas mixed function oxidase system remained unaltered. Phenobarbital reduced serum immunoreactive insulin and plasma glucose levels and decreased gluconeogenesis. Hepatic glucose phosphorylating enzyme activity increased and glucose releasing enzyme activity decreased. The demand for NADPH in drug oxidation reactions, caused by the induction phenomenon, was reflected in the elevated activities of the NADPH producing enzymes in pentose phosphate pathway and in the activities of isocitrate dehydrogenase and malic enzyme from mitochondrial oxidation reactions. Glucose metabolism of lean littermates indicated that phenobarbital induction normalizes impaired intracellular glucose handling but leaves normal glucose metabolism unaltered. Hepatic glucose production rate was related to plasma glucose, NADPH producing enzyme activities and cytochrome P450 content in the obese and lean mice.
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PMID:Effects of enzyme induction therapy on glucose and drug metabolism in obese mice model of non-insulin dependent diabetes mellitus. 250 Oct 61

DHEA, a steroid precursor of androgens and estrogens has also an inhibitory effect on several enzymes, namely on 11 beta-hydroxylase, NADH oxidase and glucose 6-phosphate dehydrogenase. The latter is the rate limiting enzyme of the pentose phosphate cycle. This metabolic pathway provides the cells with extramitochondrial NADPH and pentose phosphates. NADPH is used for the synthesis of fatty acids and steroids. Together with ribose 5-phosphate, NADPH (as coenzyme of folate reductases) is required for the synthesis of nucleic acids. A deficient production of DHEA has been found to be responsible for several diseases obesity, diabetes type 2, hypertension, arteriosclerosis and hyperuricemia as well as malignant growth (low DHEA syndrome). DHEA administration favourably modified several of these metabolic disorders. These studies were started in our laboratory in 1962 and stopped in 1976 because we were short of DHEA. At that time the response to our results was rather theoretical, but the last years a new wave of interest in DHEA called for two consecutive symposia, where important findings were presented (Paris in January and Jena in April 1989). It is a damage that this new trend, started in our laboratory, could not be pursued up to now without interruption.
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PMID:[Dehydroepiandrosterone. Renaissance after 13 years]. 252 67

The vitamin B-6 status of 15 obese and 15 nonobese black women aged 21-51 y who were not taking vitamin supplements was assessed by using plasma pyridoxal 5'-phosphate (PLP) measurements. Ages, heights, and ideal body weights of the two groups were similar as were reported energy, protein, and vitamin B-6 intakes obtained by using 24-h intake data collected on two nonconsecutive days separated by at least 1 wk. The reported vitamin B-6 intakes were 1.18 +/- 0.44 mg/d (means +/- SD). Plasma PLP levels in the obese and nonobese black women were similar; these levels were also similar to those observed previously for white obese and nonobese women having similar physical characteristics. All subjects had plasma PLP levels indicative of adequate status with one possible exception. Obesity did not affect the plasma PLP levels in these black women.
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PMID:Plasma pyridoxal 5'-phosphate concentrations in obese and nonobese black women residing near Petersburg, VA. 275 Jun 93

The adipogenic and mitogenic potentials of sera obtained from obese children before and after weight reduction and from lean control subjects were studied in clonal 3T3 L1 fibroblasts. The sera from the lean (n = 14) and obese (n = 12) children under habitual diet contained similar adipogenic activity. However, when the obese children underwent a weight-reduction program for 3 wk (600 kcal/d), the potential of their sera to stimulate glycero-phosphate dehydrogenase, an index of adipogenic activity, was significantly reduced by 32% (p less than 0.01). Similarly, the mitogenic activity of these sera decreased significantly (202 +/- 15 vs 231 +/- 27 micrograms per dish, p less than 0.01). Testing pooled sera from the different groups in cultured rat adipocyte precursor cells gave similar results. This study suggests that human childhood-onset obesity is not accompanied by increased circulatory factors involved in the formation of new fat cells. The adipogenic and mitogenic activity of sera from obese children may be influenced by long-term dietary restriction.
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PMID:Adipogenic activity in sera from obese children before and after weight reduction. 275 Jun 97

Lean and genetically obese (fa/fa) rats were fed ad libitum, or fasted for 17 h and then meal-fed for varying time intervals. During refeeding, glucose-6-phosphatase activity of lean rats declined to the low value that was present in livers of fasted obese rats and which remained unchanged in the obese group during the meal. Refeeding also resulted in increases in hepatic concentrations of glucose-6-phosphate and fructose-6-phosphate, fructose 1,6-bisphosphate, fructose-2,6-bisphosphate, alpha-glycerophosphate, pyruvate and lactate in lean and obese rats, absolute values being higher in the fasted obese than in the fasted lean group. Obese animals had higher postprandial portal blood insulin, glucose and lactate concentrations than lean animals. In spite of this, the rate of hepatic glycogen deposition was the same in both groups and was accompanied by similar glycogen synthase a levels. Following refeeding, phosphorylase was transiently inactivated in livers of lean but not of obese animals, while glycogen synthase was inactivated in both groups. The data suggest that in lean animals refeeding was associated with a stimulation of liver glycolysis, presumably by insulin; in fasted obese rats hepatic glycolysis was already in a stimulated state and was only slightly enhanced further after the meal, in keeping with their unaltered hyperinsulinaemia; there was an increased turnover of liver glycogen or a resistance to insulin stimulation of glycogen synthesis in fa/fa rats during refeeding.
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PMID:The onset of liver glycogen synthesis in fasted-refed lean and genetically obese (fa/fa) rats. 303 11

To evaluate whether changed plasma calcium binding might lead to a secondary increase of parathyroid hormone in morbid obesity, fasting measurements of serum ionized, ultrafiltrable and total calcium, calcium binding substances, and parathyroid hormone were undertaken in age- and sex-matched groups of obese (n = 44) and normal weight subjects (n = 52). The 24-hour urinary calcium excretion and clearance of creatine were also measured. Calcium binding to proteins was changed. Serum total proteins and protein-bound calcium did not differ, but serum albumin was decreased in obesity. Consequently, obese subjects did not reveal the normal dependency of protein-bound calcium upon albumin. Calcium binding to other substances was also changed. Serum phosphate and bicarbonate were decreased, while the concentrations of citrate, lactate, acetoacetate, 3-hydroxybutyrate, free fatty acids, and urate were all increased, leaving the total concentration of plasma complex-bound calcium unchanged. Nevertheless, these reciprocal changes increase the concentrations of less readily reabsorbable anions in the renal ultrafiltrate. The changed pattern of calcium binding in serum of the obese subjects may serve to explain our findings of increased urinary calcium excretion, lowering of serum ionized calcium and increased parathyroid hormone levels, changes being significantly correlated with degree of overweight.
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PMID:Increased parathyroid hormone as a consequence of changed complex binding of plasma calcium in morbid obesity. 308 Jun 52

To determine whether 1) insulin stimulates pyruvate dehydrogenase (PDH) and glycogen synthase (GS) in isolated human adipocytes and 2) adipocytes from subjects with obesity or noninsulin-dependent diabetes mellitus (NIDDM) are resistant to the effects of insulin, PDH and GS were assayed in adipocytes from 11 control, 8 obese, and 9 NIDDM subjects. Basal PDH activities were 123 +/- 20, 129 +/- 21, and 128 +/- 25 pmol pyruvate oxidized/min per 2 X 10(5) adipocytes in these groups. Insulin stimulated PDH activity to a maximum of 223 +/- 38 pmol/min per 2 X 10(5) in adipocytes from control subjects, but did not significantly increase values from obese subjects. Insulin significantly decreased PDH activity in cells from NIDDM subjects (99 +/- 20 pmol/min per 2 X 10(5) cells, P less than 0.05). PDH activity assayed with high magnesium and calcium concentrations was significantly stimulated by insulin in adipocytes from control, but not obese or NIDDM subjects. GS assayed with 1 mM glucose 6-phosphate did not differ significantly among control, obese, or NIDDM subjects (446 +/- 110, 451 +/- 156, and 291 +/- 35 pmol incorporated into glycogen, respectively). Insulin significantly stimulated glycogen synthase in all three groups (827 +/- 179, 764 +/- 177, and 569 +/- 51 pmol incorporated) to a similar extent. Glycogen synthase assayed with 10 mM glucose 6-phosphate was decreased in NIDDM (1,335 +/- 131 pmol incorporated) compared with obese or control subjects (2,512 +/- 451 and 2,239 +/- 230 pmol incorporated, respectively, P less than 0.01).
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PMID:Adipocyte glycogen synthase and pyruvate dehydrogenase in obese and type II diabetic subjects. 309 77


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