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

In order to test the relation between obesity and the secondary hyperparathyroidism found in markedly overweight subjects, 24 morbidly obese patients were studied before and after a weight loss of 35.9 kg obtained by a nutritionally adequate, intermittent very-low-calorie diet. Overweight was reduced from 98 +/- 34% to 44 +/- 19%. Serum total calcium did not change, but serum ionized calcium (Ca2+) increased from 1.22 +/- 0.04 mmol/L to 1.25 +/- 0.04 mmol/L (P less than .001). A corresponding fall was observed in serum parathyroid hormone (s-PTH), which decreased from 47.2 +/- 21.7 pmol/L to 35.2 +/- 19.4 pmol/L (P = .01). The change of s-PTH was positively associated with the reduction of body weight (r = .50, P less than .05) and with the reduction of overweight (r = .55, P less than .01). Regarding calcium binding substances, serum albumin remained low. The initially lowered serum phosphate and bicarbonate both rose (P less than .001). Plasma lactate and plasma free fatty acids (FFAs) decreased (P less than .001). The study supports our hypothesis that the change profile of calcium complexing anions in obesity interferes with the tubular reabsorption of calcium, which in turn lowers serum Ca2+, thus promoting hyperparathyroidism. Along with weight loss, concentrations of calcium complexing anions returns towards normal values and the secondary hyperparathyroidism regresses.
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PMID:Secondary hyperparathyroidism of morbid obesity regresses during weight reduction. 336 88

Risk factors for atherosclerosis are often associated with haemorheological changes. On this point, obesity (recently advocated as an independent risk factor) was not much studied and with not univocal results. We have studied 70 obese patients (BMI greater than 30) and 50 healthy subjects (BMI less than 25). Among obese 26 had no more pathologies, 29 had hypertension, 3 suffered from ischemic heart disease, 3 suffered from occlusive arteriopathy, 9 were hyperlipidemic, 10 were smokers. We determined plasma viscosity and whole blood viscosity (at haematocrit corrected to 45% too). Washed erythrocytes, poor in leucocytes and platelets and resuspended in phosphate-buffered saline, were used for study of erythrocyte viscosity and deformability. Obese patients showed raised mean blood viscosity values when compared to healthy controls (p less than 0.01); an even more significant increase (p less than 0.001) was found concerning plasma viscosity and fibrinogen. Erythrocyte viscosity and red blood cell filterability index did not show any significant difference. We found no significant correlation between viscosity values and presence of hypertension, hyperlipidemia and smoking habit among obese. In conclusion, the higher vasculopathy incidence might be caused by an increase in blood viscosity, mostly due to plasmatic component. This fact appears to be independent from the presence of atherosclerosis complications or other risk factors.
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PMID:[Hemorrheologic disorders in obese patients. Study of the viscosity of the blood, erythrocytes, plasma, fibrinogen and the erythrocyte filtration index]. 360 Nov 35

The influence of obesity on myocardial function and metabolism was studied in obese (fa/fa) and thin (Fa/Fa) Zucker rats using the isolated perfused heart as model. Cardiac performance of obese Zucker rats was not impaired. Instead, left ventricular pressure and contractility were increased as compared to controls. In agreement with these findings, creatine phosphate and the ratios of ATP/ADP and creatine phosphate creatine were elevated. The uptake and the conversion of glucose by hearts of obese Zucker rats were impaired. Insulin stimulated the uptake and oxidation of glucose. However, the responsiveness of these processes to insulin was diminished. Lipolysis of endogenous lipids was accelerated severalfold in obesity. Inhibition of fatty acid oxidation by a specific carnitine palmitoyl-transferase inhibitor, phenylalkyloxirane carboxylic acid (POCA), led to a slow rate of lipolysis, and to an acceleration of glucose oxidation and of the basal, noninsulin-dependent uptake of glucose. In the presence of POCA, insulin had, however, no additional stimulatory effect on the glucose uptake by hearts of obese rats. In contrast to hearts of ketotic, acutely diabetic rats where POCA fully restored myocardial responsiveness of glucose uptake and conversion to insulin, in hearts of obese rats only a shift in the glucose pathway from glycolytic formation of lactate and pyruvate to oxidation to CO2 was observed. Thus, POCA can be used as a tool to distinguish different forms of insulin resistance in obesity: 1) a lipid metabolism-dependent defect--presumably an inhibition of phosphofructokinase and pyruvate dehydrogenase by metabolites of fatty acid oxidation, influenced by inhibition of carnitine palmitoyltransferasei, and 2) a lipid metabolism-independent defect in the activation of uptake of glucose and glycogen synthesis by insulin not affected by POCA.
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PMID:Different types of postinsulin receptor defects contribute to insulin resistance in hearts of obese Zucker rats. 373 68

According to current concepts, soluble phosphatidic-acid phosphatase, converting phosphatidic acid into a diglyceride, is a rate-limiting enzyme in the hepatic biosynthesis of triglycerides. The present paper is the first report on this enzyme in human liver. The enzyme activity was assayed in ammonium sulphate precipitates of cytosol obtained from human liver biopsies. The activity was stimulated by preincubation with alkaline phosphatase and inhibited by Mg-ATP, suggesting that phosphorylation-dephosphorylation may be of some importance for the expression of the activity of the enzyme. When assayed under optimal conditions, the activity obtained in liver biopsies from normal-weight gallstone patients averaged 12.8 +/- 2.0 nmol min-1 (mg protein)-1 (mean +/- SEM) (n = 17). The enzyme activity was slightly higher in liver biopsies from morbidly obese subjects 16.4 +/- 2.8 nmol min-1 (mg protein)-1 (n = 14). The difference between the two groups of subjects was probably in part sex-dependent and was not statistically significant. A similar small and insignificant difference between the two groups of subjects was found when the enzyme activity was assayed in the maximally stimulated state--i.e. after incubation with alkaline phosphate. These findings suggest that an increased capacity of the soluble phosphatidic-acid phosphatase is not of major importance for the increased triglyceride synthesis known to occur in obesity. Other factors (i.e. availability of substrate and cofactors) may be of greater importance.
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PMID:Triglyceride metabolism in human liver: studies on hepatic phosphatidic-acid phosphatase in obese and non-obese subjects. 608 51

Metabolic alterations in ventromedial hypothalamus (VMH)-lesioned rats were investigated by examining daily changes of enzyme activities and urea concentrations three weeks after the operation. VMH-lesions in female adult rats caused a significant elevation in the activity of acetyl-CoA carboxylase in the liver and parametrial adipose tissue. These changes suggest an increased lipogenesis. VMH-lesions also elicited an increase in activities of glucokinase (GK), pyruvate kinase (PK) and fructose 1,6-bisphosphatase (FBPase), and a decrease in activities of phosphofructokinase (PFK), glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK) in the liver. The apparently inconsistent changes in activities of key glycolytic enzymes, GK, PK and PFK, and key gluconeogenic enzymes, G6Pase, PEPCK and FBPase in the liver may be explained by the fact that they were favorable for glucose oxidation through pentose phosphate cycle and provide NADPH for lipogenesis in the liver. Furthermore, VMH-lesions induced an increase in urea contents of the liver and serum, and elicited an increase in activity of liver tyrosine aminotransferase (TAT) and a decrease in activity of liver histidase. These changes suggest an accelerated amino acid and protein catabolism, and favor an increment in the supply of the substrate for lipogenesis. Daily rhythms of TAT, histidase activities and serum urea concentration observed in the control rats were abolished by VMH-lesions. These findings suggest that VMH-lesions elicit the loss of these daily rhythms, probably through the disturbance of the circadian rhythm of feeding behavior at this dynamic phase (three weeks after operation) of obesity.
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PMID:Shift of metabolism in rats with ventromedial hypothalamic lesions with respect to changes in daily rhythms of enzyme activity. 614 67

Obese patients who fasted during seven days were divided into four groups according to whether they received triiodothyronine (100 to 150 microgram per day), calcitonin (1 MRC unit per day), both T3 and calcitonin, or neither of these two hormones. Urinary calcium and phosphate were increased in patients receiving T3 or calcitonin. T3 given with calcitonin did not increase the calcitonin-induced calciuria but did increase the phosphaturia. The authors suggest a possible explanation for these findings. No changes in serum parathormone were recorded during fasting acidosis.
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PMID:[Urinary calcium and phosphate during fasting. Effect of various hormonal factors (author's transl)]. 628 6

The regulatory kinetic properties of phosphofructokinase partially purified from the livers of C57BL/KsJ mice were studied. The fructose 6-phosphate saturation curves were highly pH dependent. At a fixed MgATP concentration (1 mM), allosteric kinetics was observed in the range of pH studied (7.3 to 8.3) and the S0.5 values for fructose 6-phosphate decreased by about 0.2 to 0.3 mM for each 0.1-unit increment in pH. Allosteric effects on the sigmoidal response to fructose 6-phosphate: activation by AMP, NH4+, and glucose 1,6-bisphosphate, inhibition by MgATP2-, and synergistic inhibition between ATP and citrate, were all present at pH 8.0 to 8.2. Comparative kinetic studies with liver phosphofructokinase isolated from both the normal (C57BL/KsJ) and the genetically diabetic (C57BL/KsJ-db) mice of 9 to 10 and 15 to 16 weeks of age showed that the enzyme from the livers of diabetic mice exhibited decreased activity at subsaturating concentrations of fructose 6-phosphate. However, phosphofructokinase isolated from the livers of normal and genetically diabetic mice of 4 to 5 weeks of age showed no difference in kinetic properties. Thus, there appears to be a correlation between the change in properties of liver phosphofructokinase and the expression of hyperglycemia and obesity in the genetically diabetic mice. The decreased activity of liver phosphofructokinase in the older diabetic animals may well be one of the causes of the increased blood glucose levels. The results are also discussed in a general context with regard to the possible role of phosphofructokinase in the regulation of hepatic gluconeogenesis.
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PMID:Mouse (C57BL/KsJ) liver phosphofructokinase. Allosteric kinetics and age-related changes in the genetically diabetic state. 645 Feb 2

A novel anti-obesity agent which inhibits fatty acid synthesis and stimulates fatty acid oxidation is described. The hydrochloride salt of Ro 22-0654 (4-amino-5-ethyl-3-thiophenecarboxylic acid methyl ester) is a potent inhibitor of fatty acid and cholesterol synthesis in rat-isolated hepatocytes. Hepatic fatty acid synthesis was inhibited in vivo in a dose-dependent fashion with a duration of action of approximately 8 h. Adipose tissue fatty acid synthesis was also inhibited in vivo. Inhibition of fatty acid synthesis occurs without any apparent effect on several lipogenic enzymes, the tricarboxylic acid cycle, and the pentose phosphate shunt. Ro 22-0654 also stimulated fatty acid oxidation (in vitro) and lipolysis (in vivo). In long-term studies (2 months), Ro 22-0654 decreased body weight gain in Sprague Dawley and genetically-obese Zucker rats. Food intake was decreased following a single dose and for several days during chronic treatment. However, while food intake quickly returned to normal, body weight gain remained lower in treated rats. The effect on body weight gain can be ascribed to decreased total body lipid content in the absence of an effect on lean body mass. It is suggested that Ro 22-0654 may have utility in the treatment of human obesity.
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PMID:Anti-obesity activity of a novel lipid synthesis inhibitor. 653 95

The influence of alimentary obesity on the functional morphology of the adrenal cortex and glandulocytes of the testis was studied in male Wistar rats with an initial weight of 60--70 g. Analysis of some of histochemical parameters during obesity showed the disturbance of the operating mode of adrenocorticocytes and glandulocytes which manifested by changes in the activity of 3 beta-ol-dehydrogenase, glucoso-6-phosphate dehydrogenase and NADP.H-diaphorases. It was also found that obese rats had the increased adrenoglucocorticoid activity.
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PMID:[Morphological characteristics of steroid-producing glands in alimentary obesity]. 694 28

Over the last ten years a large body of information has accumulated which indicates that physiologic changes in the plasma insulin concentration are capable of affecting electrolyte transport by the kidney as well as by variety of other tissues. In the present discussion the effect of insulin on the renal handling of sodium, potassium, phosphate, and calcium is reviewed, with an emphasis on sodium transport (Table 1). An attempt is made to relate the effects of insulin on sodium metabolism to four common clinical situations: (a) hypertension and obesity, (b) sodium wasting in diabetes mellitus, (c) natriuresis of starvation, and (d) sodium retention and edema following refeeding.
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PMID:Insulin and renal sodium handling: clinical implications. 701 90


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