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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The development of obesity, hyperinsulinemia and six hepatic lipogenic enzymes in Avy/a mice were compared to that in a/a mice. Correlation between body weight, liver weight, plasma insulin concentration and activities of hepatic enzymes was analyzed. In the Avy/a mice, body weight, liver weight and plasma insulin level increased steadily as the mice aged. In the a/a mice, the change of these three parameters was much slower. Plasma insulin concentration in a/a mice did not increase until eight months of age. Compared with a/a mice, Avy/a mice had higher 6-phosphogluconate dehydrogenase and fatty acid synthetase activities at two months of age; lower citrate cleavage enzyme, glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase activities at three months of age; lower citrate cleavage enzyme and glucose-6-phosphate dehydrogenase and higher acetyl CoA carboxylase activities at five months of age; and higher malic enzyme, citrate cleavage enzyme and 6-phosphogluconate dehydrogenase activities at eight months of age. There were significant correlations between plasma insulin level and body weight and between plasma insulin level and the activities of malic enzyme and citrate cleavage enzyme in Avy/a mice. The correlation between body weight and malic enzyme and citrate cleavage enzyme activities disappeared after the analysis was adjusted for plasma insulin level.
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PMID:An analysis of the relationships among obesity, plasma insulin and hepatic lipogenic enzymes in "viable yellow obese" mice (Avy/a). 0 20

Age-related changes in hepatic and adipose glycerolipid formation have been described in Zucker rats. Glycerolipid formation was measured in vitro in the presence of [14C]glycerol-3-phosphate, palmitate, ATP, CoA, and Mg2+ by using liver and adipose tissue homogenates derived from various age groups of animals. Hepatic glycerolipid formation increased after birth to reach a peak value at 1 day of age. This period was followed by a decline in the rates of glycerolipid formation. Hepatic glycerolipid formation increased again at the time of weaning and continued to rise up to 32 days in lean rats and 42-44 days in obese rats. Obesity in rats was recognizable at the age of 32 days and was associated with increased rates of glycerolipid formation in both liver and adipose tissue. As far as the changes in hepatic glycerolipid formation and triglyceride accumulation are concerned, obese rats showed more resemblance to 1-day-old rats than to lean animals of similar age groups. Glycerolipid formation decreased in liver and increased in adipose tissue with age in both lean and obese rats. These studies suggest that hepatic and adipose tissue glycerolipid formation is significantly influenced by age and obesity in Zucker rats.
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PMID:Age-related changes in glycerolipid formation in lean and obese Zucker rats. 45 11

The effect of obesity on the activity of some enzymes of energy supplying metabolism was studied in male and female groups of different body weight, using tissue samples of m. quadriceps femoris obtained by a biopsy needle. Both obese males and females displayed a distinct tendency towards anaerobic metabolism (high lactate dehydrogenase activities). The assumption that cytoplasm has an increased capacity in the muscle of the obese for reduction syntheses is supported by the increased ratio of malate dehydrogenase to citrate synthase activities. Compared with controls, less activity of enzymes associated with fatty acid and glucose degradation (hexokinase, hydroxyacyl-CoA dehydrogenase, citrate synthase) was observed in obese males. In obese females the latter enzyme activities did not differ from those in the controls; however, lactate dehydrogenase and triosophosphate dehydrogenase activities were significantly higher. Significant inverse correlations between hexokinase and hydroxyacyl- CoA dehydrogenase activities, on the one hand, and indicators of body composition and body weight, on the other, were found in males. The female group did not display analogous significant relations between the enzymatic organization and indicators of body composition.
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PMID:Activity of some enzymes of energy metabolism in striated muscle of obese subjects with respect to body composition. 121 53

1. In biopsy samples of the lateral part of m. quadriceps femoris of 49 obese and 14 lean persons the activities of the following enzymes were investigated: triosephosphate dehydrogenase (TPDH), glycerolphosphate: nad dehydrogenase (GPDH), lactate dehydrogenase (LDH), hexokinase (HK), malate: NAD dehydrogenase (MDH), citrate synthase (CS) and hydroxyacyl-CoA dehydrogenase (HOADH). 2. The muscles of obese had an increased activity ratio of TPDH to CS and to HK, respectively, caused in muscles of female obese subjects by an increase of TPDH activity, in those of obese men rather by a decrease of CS and HK activities. 3. Cluster analysis brough to light the existence of three major groups. Group 1 (low activity-low LDH group), consisting of muscles of female obese subjects only, exhibited low activities of all enzymes investigated, that of LDH being so low as to possibly induce a serious deficiency of anerobic metabolism under working conditions. Group 2 (medium enzyme activity group) was characterized by medium enzyme activities, similar to that of lean controls (included in this group). This consisted of subjects of both sex. Group 3 (high enzyme activity group) consisted of obese of both sex. It was distinguished by high enzyme activities, especially of LDH. It is suggested that the groups of similar enzyme activity patterns might reflect different stages, types and/or genesis of obesity.
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PMID:Metabolic changes in the quadriceps femoris muscle of obese people. Enzyme activity patterns of energy-supplying metabolism. 123 24

The effect of obesity on peroxisomal beta oxidation has been studied previously only in the liver of genetically obese animals. We measured activity of peroxisomal acyl CoA oxidase (ACO) in livers, hearts and rectus femoris muscles of gold-thioglucose treated obese mice (n = 17) and control mice (n = 8). Since production of H2O2 by ACO could contribute to oxidative stress, activities of H2O2-metabolizing enzymes, catalase and glutathione peroxidase, were also measured. ACO activity was assayed using dichlorofluorescein and peroxidase as detectors of H2O2. ACO activity was higher in the obese liver and skeletal muscles than in their respective controls, while the heart ACO activity was unaltered. The activities of H2O2-metabolizing enzymes were unchanged or tended to be decreased in the obese tissues. There was a close correlation between the body weight and ACO activity in both liver and rectus femoris muscles. The ACO activity in the liver also correlated with the liver triacylglycerol content. These results suggest that the activation of peroxisomal beta oxidation occurring in both hepatic and extrahepatic obese tissues is closely linked to weight gain (i.e. non-genetic in nature), but that this does not enhance oxidative stress detected as reactive change of the defense system against H2O2.
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PMID:Peroxisomal beta-oxidation in liver and muscles of gold-thioglucose-induced obese mice: correlation with body weight. 201 Feb 57

Coronary heart disease is the leading cause of death among patients with non-insulin-dependent diabetes mellitus (NIDDM). NIDDM patients have a high frequency of dyslipidemia, which along with obesity, hypertension, and hyperglycemia may contribute significantly to accelerated coronary atherosclerosis. Because risk factors for coronary heart disease are additive and perhaps multiplicative, even mild degrees of dyslipidemia may enhance coronary heart disease risk. Therefore, therapeutic strategies for management of NIDDM should give equal emphasis to controlling hyperglycemia and dyslipidemia. The National Cholesterol Education Program recently issued guidelines for treatment of hyperlipidemia in adults including diabetic patients. Because of the unique features of diabetic dyslipidemia, however, we suggest that certain modifications in these guidelines be made to meet specific needs of diabetic patients. For example, therapeutic goals for serum cholesterol reduction should be lower in diabetic patients than in nondiabetic subjects. Particular emphasis should be given to weight reduction in NIDDM patients. In some diabetic patients, monounsaturated fatty acids may be a better replacement for saturated fatty acids than carbohydrates. The target for cholesterol lowering should include both very-low-density lipoprotein and low-density lipoprotein (LDL) (non-high-density lipoprotein) rather than LDL alone. To obtain a substantial reduction of cholesterol levels, drug therapy may be required in many patients. However, first-line drugs for nondiabetic patients (nicotinic acid and bile acid sequestrants) may be less desirable in NIDDM patients than hydroxymethylglutaryl coenzyme A (HMG CoA) reductase inhibitors and even fibric acids. In fact, HMG CoA reductase inhibitors may be the drugs of choice for NIDDM patients with elevated LDL cholesterol and borderline hypertriglyceridemia, whereas gemfibrozil appears preferable for NIDDM patients with severe hypertriglyceridemia.
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PMID:Management of dyslipidemia in NIDDM. 219 Jul 70

The purposes of the present study were to characterize the histochemical and enzymatic profiles of various hindlimb skeletal muscles, as well as to determine maximal O2 consumption (VO2max) and respiratory exchange ratios (R) during steady-state exercise in the obese Zucker rat. The changes that occurred in these parameters in response to a 6-wk training program were then assessed. Obese rats were randomly assigned to a sedentary or training group. Lean littermates served as a second control. Training consisted of treadmill running at 18 m/min up an 8% grade, 1.5 h/day, 5 day/wk for 6 wk. During week 6, VO2max and R during a steady-state run (74% max) were determined. After 2 days of inactivity, hindlimb muscles were excised, stained for fiber type and capillaries, and assayed for hexokinase, citrate synthase, cytochrome oxidase, and beta-hydroxyacetyl-CoA dehydrogenase. The obese sedentary rats demonstrated greater oxidative enzyme activities per gram of muscle tissue than their lean littermates, greater R values during submaximal exercise of the same relative intensity, and greater absolute VO2max values. Training resulted in a 20-56% increase in oxidative enzymes, a 10% increase in VO2max, and an increase in capillary density in the soleus and plantaris. There was no alteration in R values during exercise at 74% VO2max or in fiber type composition in response to exercise training. Results suggest that the muscle of the obese Zucker rat manifests a greater oxidative capacity than the muscle of its lean littermates. The apparent inability of the obese rat to increase its use of fat during submaximal exercise of the same relative intensity in response to training remains to be elucidated.
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PMID:Muscle morphological and biochemical adaptations to training in obese Zucker rats. 255 20

In earlier reports, we have described a previously unrecognized mechanism which regulates the activity of acetyl CoA carboxylase in rat liver by the control of its distribution between relatively inactive mitochondrial and active cytosolic forms. In this study, the activity, total quantity and the subcellular distribution of acetyl CoA carboxylase were determined in liver of fed and fasted (48 h) homozygous obese (fa/fa) zucker rats and homozygous lean (Fa/Fa) littermates. The results indicate that neither diet nor genetic obesity affected the total quantity of acetyl CoA carboxylase per unit weight of liver. Instead, increased activity of this enzyme in the liver of the Zucker rat was primarily due to a shift in the subcellular distribution away from relatively inactive mitochondrial forms toward active cytosolic forms. Thus, the Zucker rat appears to be yet another example illustrating the physiological importance of regulating the activity of acetyl CoA carboxylase by controlling its subcellular distribution.
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PMID:Mitochondrial storage forms of acetyl CoA carboxylase: mobilization/activation accounts for increased activity of the enzyme in liver of genetically obese Zucker rats. 256 46

A high rate of lipogenesis in obese mice plays a major role in their excessive deposition of body lipid. Inhibition of lipogenesis may decrease their obesity. Therefore, we have investigated the effects of sodium 2-n-pentadecyl-benzimidazole-5-carboxylate (M & B 35347B), an inhibitor of acetyl-CoA carboxylase, on in-vivo lipogenesis in obese and lean mice. It significantly inhibited hepatic cholesterol and fatty acid synthesis, measured using 3H2O, in both lean and obese mice, with or without a glucose load. Brown adipose tissue (scapular) lipogenesis was decreased by M & B 35347B in obese mice but not in lean mice. In white adipose tissue, M & B 35347B did not affect the rates of lipogenesis in either scapular white, inguinal or epididymal depots of obese mice, or the inguinal and scapular white depot of lean mice. However, it doubled lipogenesis in the epididymal fat pad of lean mice. After a glucose load, lipogenesis in the lean epididymal fat pad was not inhibited but that in the inguinal depot was. M & B 35347B inhibited acetyl CoA carboxylase of adipose tissue in vitro but only a small inhibition was detected after in-vivo treatment. These different responses according to type of mouse, treatment and tissue site appear to stem from differences in inhibitor concentration and the importance of acetyl CoA carboxylase as the rate-limiting enzyme of lipogenesis. The weight gain of obese mice dosed orally (200 mg M & B 35347B/kg daily) for 60 days was unaffected and they continued to deposit excess body fat. This presumably occurred because of the lack of inhibition of fatty acid synthesis in white adipose tissue.
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PMID:Effect of sodium 2-n-pentadecyl-benzimidazole-5-carboxylate (M & B 35347B), an inhibitor of acetyl-CoA carboxylase, on lipogenesis and fat deposition in obese hyperglycaemic (ob/ob) and lean mice. 289 66

It was found that in the livers of db/db mice with hyperinsulinemia, obesity and non-insulin-dependent diabetes the rates of cholesterol biosynthesis from pyruvate and, to a lesser extent, from acetate and mevalonate as well as of cholesterol ester biosynthesis from pyruvate (but not from acetate and mevalonate) are increased. Presumably, the observed changes are mediated by structural alterations in the CoA reserves, i.e., increase of free CoA to short-chain acyl-CoA and free CoA to long-chain fatty acyl-CoA indices, and of the ratio between enzymatic activities of generation and utilization of NADPH. Treatment of db/db mice with phosphopantothenate, besides eliciting changes in the CoA reserves structure towards normalization and inhibition of NADP-dependent dehydrogenases and pyruvate and 2-oxoglutarate dehydrogenase complexes, causes the diminution of cholesterol and its ester levels in the liver in the absence of any conspicuous changes in the rates of their biosynthesis from pyruvate.
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PMID:[Effect of phosphopantothenate on the biosynthesis of cholesterol and its esters from various precursors in the liver of db/db mice]. 325 47


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