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

With the aim of investigating bone mineral loss after intestinal bypass operation, bone mineral content (BMC) was measured by two-dimensional scanning photon absorptiometry on the distal part of the forearm in 23 consecutive patients who had undergone intestinal bypass operation for obesity. Eleven patients (group 1) were investigated before and 12 months after operation, and 12 (group 2), who had been operated on 2-7 years earlier, were investigated two times at an interval of 12 months. No patient received therapeutic calcium or vitamin D supply. The predominant biochemical findings postoperatively were decreased serum values of calcium, magnesium, albumin, and total protein; there was no change in inorganic phosphate or alkaline phosphatase. Mean BMC was normal in both groups postoperatively as well as in group 1 before operation; there was no significant change in mean BMC during 12 months of observation. However, in BMC measurements on extremely obese subjects, a correction for the excessive fat layer on the forearm was necessary because of different attenuation properties of fat and soft tissues. Neglect of this problem will give a systematic underestimation of BMC, and may lead to false conclusions in cross-sectional as well as longitudinal studies.
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PMID:Bone mineral content before and after intestinal bypass operation in obese patients. 722 14

Jejuno-ileostomy was performed in eight women because of severe alimentary obesity. Their calcium phosphate and bone metabolism was studied an average of 31 months post-operatively. This revealed secondary intestinal hyperparathyroidism due to an artificial malabsorption syndrome. While most of the significant metabolic factors were within normal limits, examination of calcium balance and kinetics indicated a marked disorder of calcium and bone metabolism. Calcium balance averaged-138 mg daily, corresponding to a yearly loss of skeletal mass of 4-5%.
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PMID:[Calcium and bone metabolism after jejunal bypass operation for alimentary obesity: model for a intestinally-conditioned disorder (author's transl)]. 734 80

L-Methionine (0.1 g/kg body wt) was administered to young white [n = 18; mean (+/- SD) age 20.0 +/- 1.0 y] and black [n = 12; mean (+/- SD) age 22.0 +/- 1.3 y] volunteers who had a similar lifestyle and who did not differ significantly from each other with respect to plasma folate or vitamin B-12 concentrations. Blacks, however, had significantly lower plasma pyridoxal-5'-phosphate concentrations compared with whites (P < 0.001). Fasting plasma homocysteine concentrations in blacks and whites were not significantly different. The mean (+/- SD) maximum increase in plasma homocysteine concentration measured after methionine loading was significantly lower (P < 0.01) in blacks (11.0 +/- 3.6 mumol/L) than in whites (18.0 +/- 6.2 mumol/L). Six weeks of vitamin supplementation (1.0 mg folic acid, 400 micrograms vitamin B-12, and 10 mg pyridoxine/d) reduced the mean (+/- SD) fasting plasma homocysteine concentration from 9.6 +/- 3.5 to 7.2 +/- 1.6 mumol/L in whites (P < 0.05) and from 8.4 +/- 2.4 to 5.6 +/- 1.4 mumol/L in blacks (P < 0.01). The mean (+/- SD) maximum increase in plasma homocysteine concentration after methionine loading declined from 18.0 +/- 6.2 to 11.1 +/- 2.3 mumol/L (P < 0.01) in whites, but vitamin supplementation did not have a significant effect on the methionine-load test in black volunteers. A significant race-by-time interaction shows that blacks metabolized homocysteine more effectively than did whites, which may partly explain their relative resistance against coronary heart disease despite a high prevalence of obesity, hypertension, and smoking.
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PMID:Effective homocysteine metabolism may protect South African blacks against coronary heart disease. 757 13

In the present investigation, we have compared the potential of triacylglycerol formation from sn-glycerol-3-phosphate (GP) and 2-monoacylglycerol (MG) in liver, adipose tissue and intestine from lean and obese Zucker rats. Microsomal fractions were used to measure the sn-glycerol-3-phosphate acyltransferase (GPAT), diacylglycerol acyltransferase (DGAT) and monoacylglycerol acyltransferase (MGAT) activities and homogenates were used to measure NEM-sensitive and NEM-insensitive phosphatidate phosphohydrolase (PPH) activities. In adipose tissue and liver, the GP pathway served as the major route of glycerolipid formation, with adipose tissue being 5-20-fold more active. The activities of the GP pathway enzymes increased further in response to obesity, with some degree of organ specificity. In adipose tissue of obese rats, the activities of all the pathway enzymes increased; whereas, in liver and intestine, this response was limited to PPH and GPAT, respectively. In contrast with the GP pathway enzymes, obesity in Zucker rats was not associated with alterations in the acylation of 2-monoacylglycerol. Comparison of the activities of MGAT in different intestinal segments indicated that the MG pathway was most active in the jejunum and least active in the ileum and that this pattern did not change in response to obesity. These measurements of the individual enzyme reactions provide evidence that the entire process of esterification via sn-glycerol-3-phosphate is accelerated in the various organs from obese rats and that this perturbation in lipid metabolism may contribute significantly to the increased deposition of body fat noted in this animal model.
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PMID:Triacylglycerol biosynthetic enzymes in lean and obese Zucker rats. 773 38

In different types of mammalian cells, insulin has been shown to promote the release of an inositol phosphate glycan (InsP-glycan) through the hydrolysis of a glycosyl-phosphatidylinositol (glycosyl-PtdIns). This InsP-glycan, which has been demonstrated to be taken up by intact cells, may mediate some of the biological effects of insulin. We have investigated how the insulin resistance expressed in genetically obese (fa/fa) rats affects the glycosyl-PtdIns signaling system in isolated hepatocytes compared to what occurs in hepatocytes isolated from lean (Fa/-) rats. The hepatocyte content of glycosyl-PtdIns was reduced by about 30% in obese rats, with respect to that measured in lean rats (2553 +/- 138 vs. 3334 +/- 115 dpm/mg protein; P < 0.01; n = 5). This reduction was accompanied by a marked blockade of the insulin-mediated glycosyl-PtdIns hydrolysis as well as a decrease (approximately 30%) in the rate of InsP-glycan uptake by the isolated liver cells. Obese Zucker rat hepatocytes also showed a significant decrease in the effects of both insulin and InsP-glycan on the stimulation of glycogen synthesis and the activation of glycogen synthase compared to hepatocytes isolated from lean rats. Our results demonstrate that genetic obesity in Zucker (fa/fa) rats is associated with an impairment of the glycosyl-PtdIns-dependent insulin signaling system.
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PMID:Insulin resistance in genetically obese (fa/fa) rats: changes in the glycosyl-phosphatidylinositol signaling system in isolated hepatocytes. 811 90

Alterations in calcium metabolism have been associated with cardiovascular risk factors. An altered binding of calcium to plasma proteins and raised levels of parathyroid hormone (PTH) have been described in morbid obesity. In the present study, indices of mineral metabolism were related to obesity (body mass index, BMI) and fat distribution (waist to hip ratio, w/h) in 194 subjects with a wide range of BMI and w/h. The ratio of total serum calcium to plasma ionized calcium (Ca2+) was found to be significantly correlated to both BMI (r = 0.20, P < 0.02) and w/h (r = 0.22, P < 0.005). Serum phosphate was also correlated to both of the indices of obesity in an inverse way (r = -0.24, P < 0.0008 for BMI and r = -0.33, P < 0.0001 for w/h). These relationships were still significant when the influences of age, sex and serum creatinine were included in the multiple regression analysis. This kind of analysis also disclosed that w/h was superior to BMI as a determinant of serum phosphate and the total calcium/Ca2+ ratio in serum. PTH was not significantly correlated to any of the indices of obesity. In conclusion, fat distribution rather than obesity per se was found to be associated with an altered mineral metabolism.
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PMID:On the relationships between mineral metabolism, obesity and fat distribution. 835 38

Previous studies from our laboratory demonstrate that polyamines, namely spermine and spermidine, stimulate adipose triacylglycerol formation from the sn-glycerol-3-phosphate pathway by activation of several enzymes from this pathway, including sn-glycerol-3-phosphate acyltransferase, Mg(2+)-dependent phosphatidate phosphohydrolase and diacylglycerol acyltransferase. Since obesity in Zucker rats was associated with increased accumulation of adipocyte triacylglycerols, we have examined the relationship between changes in the activities of various triacylglycerol synthetic enzymes and the endogenous concentrations of spermine and spermidine in the adipose tissues from lean and obese animals. As compared with lean rats, the adipocytes from obese rats showed a 4-fold rise in the concentration of spermine and spermidine which was accompanied by 4- to 14-fold increases in the activities of various triacylglycerol synthetic enzymes, including Mg(2+)-dependent phosphatidate phosphohydrolase. These studies suggest that obesity in Zucker rats is associated with the activation of various adipose triacylglycerol synthetic enzymes resulting from increased concentrations of endogenous spermine and spermidine.
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PMID:Relationship between adipose polyamine concentrations and triacylglycerol synthetic enzymes in lean and obese Zucker rats. 903 Aug 89

Leptin is a protein secreted by adipocytes that is important in regulating appetite and adiposity. Recent studies have suggested the presence of leptin receptors in the arcuate nucleus of the hypothalamus (ANH). Neonatal administration of monosodium glutamate (MSG) damages the ANH, resulting in obesity and neuroendocrine dysfunction. Neonatal administration of MSG was utilized to test the hypothesis that the anatomic site for many of leptin's actions is the ANH. Female control (n = 6) and MSG-treated rats (n = 7) were implanted for 14 days with osmotic minipumps containing phosphate-buffered saline or leptin (1 mg.kg-1.day-1). Leptin suppressed (P < 0.05) body weight gain in controls but did not suppress weight gain in MSG-treated rats. Leptin decreased (P < 0.05) fat depots in controls but had no effect in MSG-treated rats. Night feeding was suppressed (P < 0.05) in leptin-treated control rats. MSG-treated rats showed a suppression in food intake that was of a smaller magnitude and appeared later in the course of leptin treatment. These findings suggest that leptin mediates some physiological actions related to fat mobilization via receptors located in the ANH.
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PMID:Attenuation of leptin-mediated effects by monosodium glutamate-induced arcuate nucleus damage. 925 97

Glucose-6-phosphatase (Glu-6-Pase) catalyzes the terminal step of gluconeogenesis, the conversion of glucose 6-phosphate (Glu-6-P) to free glucose. This enzyme activity is thought to be conferred by a complex of proteins residing in the endoplasmic reticulum (ER), including a Glu-6-P translocase that transports Glu-6-P into the lumen of the ER, a phosphohydrolase catalytic subunit residing in the lumen, and putative glucose and inorganic phosphate transporters that allow exit of the products of the reaction. In this study, we have investigated the effect of adenovirus-mediated overexpression of the Glu-6-Pase catalytic subunit on glucose metabolism and insulin secretion, using a well differentiated insulinoma cell line, INS-1. We found that the overexpressed Glu-6-Pase catalytic subunit was normally glycosylated, correctly sorted to the ER, and caused a 10-fold increase in Glu-6-Pase enzymatic activity in in vitro assays. Consistent with these findings, a 4.2-fold increase in 3H2O incorporation into glucose was observed in INS-1 cells treated with the recombinant adenovirus containing the Glu-6-Pase catalytic subunit cDNA (AdCMV-Glu-6-Pase). 3-[3H]Glucose usage was decreased by 32% in AdCMV-Glu-6-Pase-treated cells relative to controls, resulting in a proportional 30% decrease in glucose-stimulated insulin secretion. Our findings indicate that overexpression of the Glu-6-Pase catalytic subunit significantly impacts glucose metabolism and insulin secretion in islet beta-cells. However, INS-1 cells treated with AdCMV-Glu-6-Pase do not exhibit the severe alterations of beta-cell function and metabolism associated with islets from rodent models of obesity and non-insulin-dependent diabetes mellitus, suggesting the involvement of genes in addition to the catalytic subunit of Glu-6-Pase in the etiology of such beta-cell dysfunction.
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PMID:Adenovirus-mediated expression of the catalytic subunit of glucose-6-phosphatase in INS-1 cells. Effects on glucose cycling, glucose usage, and insulin secretion. 931 82

This report describes a 37-year-old man presenting with a gait disturbance due to spastic paraparesis. Physical findings showed typical features of Albright's hereditary osteodystrophy, including short stature, obesity, brachydactyly and dental hypoplasia. He was diagnosed as having pseudohypoparathyroidism type Ia, on the basis of his hypocalcaemia, hyperphosphataemia, increased plasma level of parathyroid hormone (PTH), and the unresponsiveness to exogenous PTH loading of his urinary excretion of both nephrogenous cyclic adenosine monophosphate and phosphate. Magnetic resonance imaging and myelographic computed tomographic scans clearly demonstrated severe compression of the spinal cord at T 9/10 by tumour-like ossifications of the paravertebral ligaments. Neurosurgical decompression therapy was, therefore, performed to alleviate his spastic paraparesis. This was a rare case of pseudohypoparathyroidism complicated with spinal cord compression caused by ectopic ossification of the ligaments.
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PMID:Spinal cord compression by heterotopic ossification associated with pseudohypoparathyroidism. 942 70


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