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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To determine the effect of weight loss on serum high-density lipoprotein cholesterol (HDL-C), we measured serum HDL-C as well as total cholesterol and triglycerides in 65 subjects 56 women and 9 men, mean age 41.1 +/- 1.5 (+/- SEM yr) before and after a weight reduction program. At entry into the program there was a significant correlation between HDL-C and several indices of overweight--relative weight, body mass index and sum of skinfold thickness. For all subjects, despite a significant weight loss of 4.5 kg or 5.8% of initial body weight and significant decrease in sum of skinfold thickness, there was no significant increase in HDL-C or correlation between changes in HDL-C and change in body weight or skinfold thickness. For women, but not men, a weak negative correlation between change in HDL-C and change in weight or percentage change in weight was observed. However, in the subset of women who were current cigarette smokers a significant (p less than 0.01) correlation was observed between change in HDL-C and change in weight (r = -0.876) and percentage change in weight (r = -0.881). Thus a modest weight loss is not usually associated with a significant increase in serum HDL-C concentration except in cigarette smoking women.
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PMID:Relationship of weight loss and cigarette smoking to changes in high-density lipoprotein cholesterol. 728 4

The lipid composition of fasting gallbladder bile obtained under standardized conditions was determined in healthy controls and in patients with hyperlipoproteinemia without gallstones. Altogether 23 normolipidemic controls (10 males and 13 females) and 50 hyperlipidemic patients (31 type IIa, 7 type IIb, and 12 type IV) were studied; all were less than 15% overweight. The cholesterol saturation averaged 96 +/- 5% (mean +/- SEM) in the controls, and 10 of them had bile supersaturated with cholesterol. There was no difference between males and females. An increased saturation with age was seen in females. A normal biliary cholesterol saturation (102 +/- 3%) was found in patients with hyperlipoproteinemia type IIa; this was true also for the subgroup with established familial hypercholesterolemia. All patients with hyperlipoproteinemia type IIb and 10 of those with type IV had saturated bile (135 +/- 8% and 121 +/- 6%, respectively). The results suggest an association between certain forms of hyperlipoproteinemia and the development of supersaturated bile. Since fasting gallbladder bile supersaturated with cholesterol is considered to precede gallstone formation, the present results may explain previous findings of an increased prevalence of gallstone disease in patients with hypertriglyceridemia.
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PMID:Biliary lipid composition in normo- and hyperlipoproteinemia. 738 Feb 28

The third National Health and Nutrition Examination Survey (NHANES III) was conducted to assess the health and nutritional status of the US population. As part of the nutritional status assessment, reliable 24-h dietary recalls were collected for 14,801 examined persons. Mean (+/- SEM) energy intakes are reported for persons aged > or = 2 mo by age, sex, and race-ethnicity. Males had higher mean energy intakes than did females. Energy intakes peaked during late adolescence and young adulthood and declined thereafter. Energy intake patterns were similar among non-Hispanic whites, non-Hispanic blacks, and Mexican Americans. Underreporting was addressed by computing a ratio of energy intake (EI) to estimated basal metabolic rate (BMRest). This ratio (EI:BMRest) was 1.47 for adult males and 1.26 for nonpregnant adult females. Overweight adults had a lower mean EI:BMRest (1.09 in females and 1.28 in males). Underreporting in food consumption surveys remains problematic among females and overweight persons.
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PMID:Total energy intake of the US population: the third National Health and Nutrition Examination Survey, 1988-1991. 748 24

Recent evidence suggests that the postprandial hyperglycaemia in impaired glucose tolerance is primarily due to impaired suppression of basal hepatic glucose output. This in turn appears to be secondary to decreased first phase insulin secretion, although decreased hepatic insulin sensitivity, which is a feature of non-insulin-dependent diabetes mellitus, might also play a role. Eight mildly overweight subjects with impaired glucose tolerance and eight closely matched control subjects with normal glucose tolerance underwent an intravenous glucose tolerance test to assess first phase insulin secretion. Insulin sensitivity was examined by a 150-min hyperinsulinaemic-euglycaemic clamp. Somatostatin was infused from 150 min to suppress endogenous insulin secretion, and glucagon and insulin were replaced by constant infusion. Glucose with added dideuterated glucose (labelled infusion technique) was infused to maintain euglycaemia. First phase insulin secretion (delta 0-10 min insulin area divided by delta 0-10 min glucose area) was significantly decreased in the subjects with impaired glucose tolerance (median [range]: 1.2 [0.2-19.4] vs 9.1 [2.6-14.5] mU.mmol-1; p < 0.01). During the clamp, circulating insulin (93 +/- 8 [mean +/- SEM] and 81 +/- 10 mU.l-1) and glucagon (54 +/- 4 and 44 +/- 6 ng.l-1) levels were comparable. Total glucose disposal was decreased in subjects with impaired glucose tolerance (2.78 +/- 0.27 vs 4.47 +/- 0.53 mg.kg-1.min-1; p < 0.02), and was primarily due to decreased non-oxidative glucose disposal. However, hepatic glucose output rates were comparable during the clamp (0.38 +/- 0.10 and 0.30 +/- 0.18 mg.kg-1.min-1).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Peripheral and hepatic insulin sensitivity in subjects with impaired glucose tolerance. 767 92

A consequence of short-term very-low-energy diets (VLEDs) in lean subjects is reactive hypoglycemia. We therefore tested the responses of overweight women on prolonged (14 d) VLEDs. Subjects lost 4.8 +/- 0.2 kg (mean +/- SEM, n = 13, P < 0.001). Group A (n = 6) was challenged with an oral-glucose-tolerance test (OGTT) and group B (n = 7) with an oral-sucrose-tolerance test (OSTT) on days 1 and 14. In group A, mean nadir plasma glucose after the OGTT was lower on day 14, 3.75 +/- 0.16 vs 4.7 +/- 0.19 mmol/L (P < 0.01), because of an accelerated rate of glucose decline (RGD, 26.7 +/- 3.3 vs 17.2 +/- 3.9 mumol.l-1.min-1, P < 0.05) late in the OGTT. Plasma insulin was also lower (P < 0.03) and the VLED suppressed two growth hormone (GH) peaks on day 14 (P < 0.05 for each). In group B on day 14, a greater RGD was also observed late in the OSTT, 16.9 +/- 4.1 vs 6.5 +/- 2.0 mumol.L.min-1 (P < 0.03). GH peaks were also significantly suppressed. We conclude that a VLED results in altered glucose regulation late after carbohydrate loading, characterized by an accelerated decline in plasma glucose and GH suppression. Patients on a VLED may be at risk for abnormally low plasma glucose concentrations when ingesting high carbohydrate loads.
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PMID:Very-low-energy diets alter the counterregulatory response to falling plasma glucose concentrations. 784 77

Protein S is a vitamin K-dependent glycoprotein acting as a cofactor for activated protein C and thereby exerting an antithrombotic effect. When compared to values recorded in the 10 healthy normal weight normolipidemic control subjects (80.1% +/- 5.16; mean +/- SEM), plasma protein S-antigen (PS:Ag) level was found to be significantly (p < 0.01) decreased in the 11 patients with decompensated cirrhosis of the liver (54.72% +/- 4.89) and in the 12 surgical patients in critical condition (59.2 +/- 4.96), while obviously (p < 0.001) increased plasma levels were noted in the group including 20 overweight and hyperlipidemic subjects (113% +/- 3.1). Since the low PS:Ag level was associated with a decreased serum cholinesterase (CHE) activity, while both plasma PS:Ag and serum CHE activity were increased in overweight and hyperlipidemic subjects it is considered that impaired or respectively enhanced hepatic protein synthesis is at least partially responsible for changes affecting this antithrombotic plasma protein.
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PMID:Plasma protein S-antigen (PS:Ag) in selected disease states. 808 8

The effect of phenylpropanolamine (PPA), a noncatecholamine sympathomimetic weight-loss agent, on energy expenditure (EE) and substrate oxidation was measured in a respiratory chamber in 24 overweight women after 4 d of treatment (PPA or placebo) during weight maintenance and after 7 wk of treatment on a hypoenergetic diet (70% of measured baseline 24-h EE). Twelve women (37 +/- 2 y, 74 +/- 6 kg, 33 +/- 1% body fat) were randomly assigned to the PPA group [75 mg osmotic release oral system (OROS)-PPA/d] and 12 (mean +/- SEM: 38 +/- 2 y, 79 +/- 1 kg, 37 +/- 1% body fat) to the placebo group. Baseline measurements of 24-h EE (7849 +/- 226 vs 7834 +/- 142 kJ/d), basal metabolic rate (BMR) and 24-h respiratory quotient (RQ) were comparable between PPA and placebo groups. After 4 d of treatment, there was no significant effect of PPA on 24-h EE, BMR, and 24-h RQ compared with placebo. Over the 7-wk diet period, however, the PPA group (n = 8) had greater weight loss than the placebo group (n = 10): -5.0 +/- 0.5 vs -3.0 +/- 0.4 kg (P < 0.05). The changes in 24-h EE and 24-h RQ over the 7 wk were not different between the groups. We conclude that weight loss is enhanced by OROS-PPA, but this change was not explained by changes in 24-h EE or 24-h RQ. The small number of subjects may have hindered detection of subtle differences in energy metabolism.
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PMID:Effect of phenylpropanolamine on energy expenditure and weight loss in overweight women. 842 78

C57BL/6J (B/6J) mice are genetically predisposed to become overweight and develop hyperglycemia if raised on a high fat diet. The purpose of the present study was to explore the effect of dietary supplementation of L-glutamine (Gln), an inhibitor of fatty acid oxidation, on the development of hyperglycemia and excessive weight gain. Groups of 10 age- and weight-matched male B/6J mice were raised on one of four diets: 1) a low fat, low sucrose (LL), studied separately, 2) a high fat, low sucrose (HL) diet alone, 3) high fat, low sucrose supplemented with L-glutamine (HL+Gln) and 4) high fat, low sucrose supplemented with L-alanine (HL+Ala). Energy intake, body weight, plasma glucose and insulin concentrations were monitored over time. We found no difference in energy intake per unit body weight between any groups after the first 2 wk of feeding. However, the mean +/- SEM for body weight (27.1 +/- 0.6 g) of the LL group measured at 16 wk was lower (P < 0.05) than that of the HL group at 37.9 +/- 1.9 g. Also, after 5.5 mo, the mean +/- SEM for plasma glucose and insulin concentrations in the LL group of mice were 6.9 +/- 0.4 mmol/l and 146 +/- 30 pmol/l, which were lower (P < 0.05) than those in the HL group at 10.1 +/- 0.9 mmol/l and 438 +/- 84 pmol/l, respectively. Although both amino acids caused a 10% reduction (P < 0.05) in body weight compared with HL feeding at wk 16, only Gln supplementation resulted in persistent reductions in both plasma glucose and insulin concentrations over 5.5 mo. In another experiment, when Gln was added to the high fat (HL) diet of heavy hyperglycemic animals for 2 mo, body weight gain, hyperglycemia and hyperinsulinemia were attenuated. In conclusion, supplementing glutamine to a high fat diet reduces body weight and attenuated hyperglycemia and hyperinsulinemia in B/6J mice.
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PMID:L-glutamine supplementation of a high fat diet reduces body weight and attenuates hyperglycemia and hyperinsulinemia in C57BL/6J mice. 855 12

The feasibility of simultaneous dual-isotope myocardial perfusion imaging was assessed using a ca. 12 mCi dose of technetium-99m sestamibi (MIBI) and ca. 3 mCi thallium-201. Planar and single-photon emission tomographic (SPET) data from 40 patients (41 studies) imaged with both a single- and a dual-isotope protocol were analyzed. Rest injected 201T1 (pure-T1) images were acquired using 20% windows at 70 and 166 keV about 15 min after the 201T1 injection. Patients were then stressed, and at peak stress 99mTc-sestamibi was injected. About 30 min later 99mTc data were recorded with a 20% window center at 140 keV, and simultaneous 201T1 (dual-T1) data were recorded with a single 20% window centered at 80 keV. Total myocardial counts based on SPET data in the dual-T1 images were increased by 18.61% +/- 2.91% (SEM) (range: -12.8% to 84.1%) compared to pure-T1 images. Region of interest analysis revealed the greater increase in counts in the apical region and the least in the lateral wall. Pure T1 and dual-T1 images were visually evaluated for image quality (IQ) on a five-point scale (0 = unacceptable to 4 = excellent). Dual-T1 IQ was lower than that of pure-T1 in 61% of cases, and similar in 37% (12% of the pure-T1 and 41% of the dual-T1 images fell into the 0 and 1 categories). Thallium perfusion abnormalities were of similar extent in 70% of segments, less severe in 18%, and more severe in 12%. There was an inverse correlation with patient weight, such that patients weighing more than 180 lbs had substantially worse images than those below this cutoff value. While dual-tracer images are of lower quality, they are interpretable if the patient is not severely overweight.
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PMID:Feasibility of simultaneous dual-isotope myocardial perfusion acquisition using a lower dose of sestamibi. 914 65

Increased dietary sodium intake has been associated with an increase in blood pressure as well as a decrease in insulin-mediated glucose disposal in young healthy adults. The purpose of this study was to determine whether dietary sodium intake is associated with changes in oral glucose tolerance, insulin sensitivity, and blood pressure in older, sedentary, overweight hypertensives. Eight older (70.0 +/- 1.4 years, mean +/- SEM), overweight (40.2 +/- 3.1% body fat), mildly hypertensive (151 +/- 8/82 +/- 2 mm Hg) patients with a fasting plasma glucose < 7.8 mmol/L were studied after 2 weeks on low (3 g/day) and 2 weeks on high (10 g/day) sodium diets. To examine carbohydrate metabolism we performed a 2 h oral glucose tolerance test and a two-dose (240 and 600 pmol/m2/min) hyperinsulinemic-euglycemic clamp at the end of each sodium diet. High sodium intake was associated with a significantly greater urinary sodium excretion (364 +/- 45 mmol/day v 112 +/- 21 mmol/day; P < .0001). The increase in dietary sodium from low to high did not result in significant differences in fasting plasma glucose (6.0 +/- 0.2 v 5.8 +/- 0.1 mmol/L, P = .20) or insulin (72.5 +/- 7.8 v 69.9 +/- 12.4 pmol/L, P = 0.71) levels or in the glucose (374.0 +/- 50.8 v 493.2 +/- 45.0 mmol/min/L, P = .12) and insulin (43,783 +/- 10,278 v 44,110 +/- 12,392 pmol/min/L, P = .96) areas determined during the oral glucose tolerance test. Similarly, there was no effect of dietary sodium on insulin-mediated glucose disposal at low (5.87 +/- 1.02 v 5.60 +/- 0.94 mg/kgLBM/min, P = .36) or high (12.15 +/- 1.49 v 11.91 +/- 1.49 mg/kgLBM/min, P = .64) insulin infusion rates. Our findings suggest that, in insulin resistant hypertensives, increased dietary sodium does not affect either glucose or insulin responses during an oral glucose tolerance test or glucose disposal during a hyperinsulinemic euglycemic clamp.
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PMID:Effect of dietary sodium on insulin sensitivity in older, obese, sedentary hypertensives. 932


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