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

The two-compartment model presented here suggests that weight maintenance can be achieved by a regulation of food intake geared primarily toward the maintenance of stable glycogen levels, rather than toward the preservation of the overall energy balance. This concept is reminiscent of the glucostatic theory of food intake regulation proposed by Mayer. It is viewed here as being linked to changes in the body's carbohydrate stores, which represent an integration of carbohydrate and lipid fluxes, rather than to changes in blood glucose levels, whose substantial variations during the day are dependent on various circumstantial events. The model illustrates that the fat to carbohydrate ratio of the diet may have considerable potential influence on steady state body composition, even though carbohydrates and fats are both able to meet the body's energy substrate requirements. It appears that failure of appropriately reducing the range within which glycogen levels are maintained when the diet's fat content rises will require an expansion of the adipose tissue mass to raise FFA levels and fat oxidation to a rate commensurate with the proportion of fat in the diet. Maintenance of glycogen reserves below their level of saturation is made less likely by the high palatability and ubiquitous availability of foods in affluent societies. Thus, one can understand the high incidence of obesity among populations consuming mixed diets with a relatively high fat content, without having to attribute this to some defect(s) in the mechanism(s) controlling food intake.
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PMID:The difference in the storage capacities for carbohydrate and for fat, and its implications in the regulation of body weight. 330 Apr 76

Male Sprague-Dawley IVA-SIV rats were compared to male Sprague-Dawley Charles River rats of the same age, body weight, and daily food intake. The IVA-SIV rats demonstrated hypertriglyceridemia (182 +/- 9.4 v 131 +/- 9.4 mg/dL, P less than 0.001), associated with increased fasting plasma glucose (115 +/- 3 v 84 +/- 2 mg/dL, P less than 0.001), and plasma insulin (35 +/- 5 v 19 +/- 2 microU/mL, P less than 0.001) levels. Furthermore, IVA-SIV rats responded to an oral glucose load with higher plasma glucose and insulin levels. Very-low-density lipoprotein (VLDL)-triglyceride (TG) turnover studies were performed, documenting a higher TG production rate, which correlated with the plasma TG concentrations, (r = 0.58, P less than 0.01) in the IVA-SIV rats. Since lipoprotein lipase activity in both adipose tissue and muscle was not significantly different in the two groups of rats, it appears that the hypertriglyceridemia in IVA-SIV rats is due to increased VLDL-TG secretion, associated with hyperglycemia, hyperinsulinemia, and increased plasma FFA levels. The IVA-SIV rats provide a model of endogenous hypertriglyceridemia, independent of obesity.
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PMID:Pathogenetic mechanisms of the endogenous hypertriglyceridemia in a nonobese rat model. 351 53

Fasting and postprandial plasma concentrations of glucose, FFA, insulin, glucagon, and GH concentrations were determined in 10 nonobese and 10 obese subjects with normal glucose tolerance. Measurements were made at 0800 h (after a 14-h fast) and at hourly intervals from then until 1600 h. During this time period all individuals ate breakfast at 0800 h (20% of total daily calories) and lunch (40% of total daily calories). Although plasma glucose concentrations were similar throughout the 8-h period in the 2 groups, plasma insulin concentrations were significantly (P less than 0.001) higher in the obese individuals. However, despite the presence of hyperinsulinemia, the obese group also had higher (P less than 0.001) plasma FFA concentration throughout the day. On the other hand, both the absolute and the relative declines in plasma FFA concentration after meals were similar in the 2 groups. Since plasma glucagon and GH concentrations were similar in the 2 groups, altered production of these lipolytic hormones was not responsible for the elevated plasma FFA levels in the obese individuals. These data document the presence in obese individuals of a disassociation in their ability to maintain normal plasma glucose as opposed to plasma FFA homeostasis, and indicate that the increase in plasma FFA concentrations in obesity occurs in the presence of hyperinsulinemia and is not related to abnormalities of either glucagon or GH secretion.
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PMID:Effect of obesity on ambient plasma glucose, free fatty acid, insulin, growth hormone, and glucagon concentrations. 352 20

Insulin resistance is frequently observed in obese subjects. The present work was initiated to study its relationship with the increased lipid metabolism generally observed in obesity. A first group of five obese subjects (146 +/- 10% of their ideal body weight [IBW] with normal glucose tolerance was submitted to a 75-g oral glucose tolerance test (OGTT) as a control and during an intralipid infusion (20% fat emulsion, 1 mL/min, started 90 minutes prior to the glucose load). Lipid and glucose oxidation were measured by continuous indirect calorimetry. The significant rise over control conditions in both plasma FFA and lipid oxidation rate during the lipid infusion was accompanied by a marked decrease in glucose tolerance (two hours venous plasma glucose: 151 +/- 12 during intralipid infusion v 110 +/- 3 mg/dL, P less than .01) together with a rise of the plasma insulin curve. Glucose oxidation was significantly decreased. A second group of five obese subjects (146 +/- 7% of their IBW) with impaired glucose tolerance was submitted to a similar OGTT, as a control, and during an infusion of beta-pyridyl-carbinol, a nicotinic acid derivative, to lower FFA. Both plasma FFA and lipid oxidation rates were decreased already prior to the OGTT. The previously impaired glucose tolerance was normalized (two hours venous plasma glucose: 129 +/- 13 during the beta-pyridyl-carbinol infusion v 172 +/- 7 mg/dL, P less than .01), and the insulin curve lowered. Glucose oxidation was increased during the early phase of the OGTT.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Metabolic factors in the insulin resistance in human obesity. 354 14

Recent studies have shown that adipose tissue metabolism varies in different regions. Thus, hormonal responsiveness and sensitivity to both lipolytic and anti-lipolytic agent is increased in abdominal as compared to femoral cells. Abdominal obesity is also associated with greater aberrations in metabolism than peripheral obesity. The increased lipolytic response in abdominal fat cells may lead to higher FFA concentrations, which may attenuate both glucose uptake and insulin clearance by the liver.
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PMID:Regional differences in adipocyte metabolism and possible consequences in vivo. 390 44

There is a 'futile' cycle of unknown significance operating at a very rapid rate (about 40 percent that of the total central fat droplet's daily turnover rate) in white adipose tissue of normal mice. The futile cycle may be measured and studied because it occurs in a region of the adipose tissue that has poor anatomical contact with the capillaries coupled with a high affinity of the adipocytes, plasma membranes for the FFA in the ECF. The cycle is drastically inhibited in mice bearing the Ehrlich ascites carcinoma, a transplantable tumor; the inhibition is associated with a 20-fold increase in the FFA pool size of the epididymal fat pad (measured directly) and a 70 percent reduction in the TGFA pool that is involved in the cycle (estimated indirectly from kinetic measurements). However, the mass of TGFA in the central lipid droplet was being conserved in the tumor-bearing mice during this study. The TGFA pool involved in the cycle represents only about 1 percent of the total adipose tissue TGFA. The relation of this futile cycle to adipose TGFA turnover, plasma FFA turnover and oxidation to CO2, dietary sources of TGFA, and the loss (and preservation) of body fat in cancer-bearing animals was considered in terms of a simple model. Although the significance of the altered futile cycle is unknown, the new approach described here, coupled with other quantitative tracer and non-tracer measurements, may prove useful in understanding factors that lead to obesity or body fat loss.
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PMID:In vivo tracer studies of perturbed fatty acid transport and metabolism in adipose tissue. 406 21

Because increases in adipose tissue lipoprotein lipase (ATLPL) may be important in the pathogenesis of obesity, the response of ATLPL to insulin during maintenance of euglycemia was examined in 22 obese and 8 normal weight subjects. Basal levels of ATLPL per g fat tissue for the obese and control groups were 18.7 +/- 2.0 (+/- SEM) and 9.6 +/- 2.7 neq/g X min, respectively. Insulin and glucose infusion rapidly produced antilipolysis in both groups, as evidenced by large falls in FFA by 20 min. When the responses of ATLPL in absolute change from basal were compared between the obese and control groups, no significant differences were found. However, because of the higher baseline ATLPL values in the obese subjects, the percent change in ATLPL from basal was significantly blunted at the 80 (P = 0.02), 180 (P less than 0.05), and 360 (P = 0.005) min timepoints compared to those in the normal subjects. By 3 h into the infusion, the control group had a significant rise in ATLPL above the basal level (4.2 +/- 1.3 ngq/g X min; P = 0.01), whereas the obese group did not (2.3 +/- 1.9 neq/g X min; P = NS). However, by 6 h, the ATLPL per g response above baseline was significantly increased in both normal (19.2 +/- 6.5 neq/g X min; P = 0.01) and obese subjects (9.8 +/- 2.3; P less than 0.001). Because adipose cell size was greater in obese subjects, data were also expressed per 10(6) cells. Basal ATLPL per 10(6) cells [11.8 +/- 1.7 neq/10(6) cells X min (obese); 3.4 +/- 0.9 neq/10(6) cells X min (normal)] was a function of cell size (rs = 0.713; P less than 0.001), body mass index (rs = 0.565; P less than 0.005), and basal insulin levels (rs = 0.434; P less than 0.05). As with the ATLPL per g response, the increases in ATLPL per 10(6) cells above basal were significant at both the 3 and 6 h marks for the normal subjects, but only at the 6 h timepoint for the obese group. Both steady state insulin levels [342 +/- 24 microU/ml (obese); 251 +/- 27 microU/ml (normal)] and the glucose infusion rates needed to maintain euglycemia [319 +/- 23 mg/m2 X min (obese); 312 +/- 33 mg/m2 X min (normal)] did not correlate with changes in ATLPL. Thus, insulin responsiveness of ATLPL in obese subjects was delayed but preserved. This phenomenon may be important in maintenance of the obese state.
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PMID:Insulin responsiveness of adipose tissue lipoprotein lipase is delayed but preserved in obesity. 638 39

Intravenous glucose tolerance tests were performed in 33 obese and 12 nonobese children. In addition to the glucose disappearance rate the changes in response to the glucose load in plasma insulin, FFA, glycerol, cholesterol, triglyceride, lactate and pyruvate were examined. The relationship between biochemical parameters and the glucose disappearance rate was also studied. 1. Reduced glucose tolerance, basal and glucose-induced hyperinsulinaemia were frequent in the obese children. 2. Normal or reduced glucose tolerance in spite of the apparent hyperinsulinaemia and the negative correlation between fasting insulin level and KG in the nonhypertriglyceridaemic obese group was the marker of insulin resistance in overweight children. 3. The reduced elevation of FFA in the 2nd hour of the intravenous glucose tolerance test might be the sign of an impaired lipolysis in obesity. 4. The significant negative correlation found between KG, fasting FFA and triglyceride levels in certain obese subgroups suggested the importance of FFA and triglyceride in the regulation of peripheral glucose utilization.
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PMID:Intravenous glucose tolerance test in childhood obesity: metabolite levels and their relation to glucose utilization rate (KG). 675 63

Thirty hospitalized, severely obese patients (40 +/- 2 yr, 82 +/- 4 percent weight excess) were submitted to a 13-d protein-supplemented fast (PSF) with 70 g milk proteins/d (1.26 MJ or 300 kcal). The mean weight loss during PSF was 5.4 +/- 0.3 kg corresponding to 422 +/- 39 g/d. Comparison of the urinary nitrogen excretion with daily protein intake revealed that the nitrogen balance was equilibrated during PSF. Blood glucose decreased moderately but significantly during the whole PSF period whereas plasma insulin was only reduced during the first 9 d and tended to rise thereafter. Plasma FFA increased rapidly and remained elevated until the end of the study (+ 60 per cent); serum total cholesterol and plasma triglycerides showed a 26 and a 35 per cent decrease respectively. Basal plasma glucagon was slightly increased. Due to the low sodium intake (42 mmol/d) urinary sodium excretion dropped rapidly. Simultaneously both systolic (-13 mmHg) and diastolic (-7 mmHg) arterial blood pressure decreased significantly. The biological tolerance was good: metabolic acidosis was prevented with sodium bicarbonate, excessive rise in serum uric acid was corrected with allopurinol and a marked decrease in serum potassium was avoided with an appropriate dose of spironolactone. Twenty-six patients could be weighed 6 to 15 months after PSF: 12 showed a further weight reduction (6.6 +/- 1.6 kg) and seven a discrete weight gain (1.0 +/- 0.4 kg). Thus, PSF was well accepted and was profitable in 19 out of our 30 patients. It should be restricted to cases of severe and refractory obesity and performed under careful medical supervision.
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PMID:Hormonal and metabolic adaptation to protein-supplemented fasting in obese subjects. 704 25

The effects of obesity and gender on plasma catecholamine levels were studied in 10 lean men, 10 lean women, and 10 obese women. Measurements (mean +/- SE) were obtained sequentially after 30 min of bedrest, 10 min of standing, and 5 min of sustained handgrip, and following 15 min of rest while standing. The supine plasma norepinephrine (NE) levels were comparable among the 3 groups, whereas plasma epinephrine (E) was lowest in obese women (14 +/- 2 pg/ml), intermediate in lean women (19 +/- 2 pg/ml), and highest in lean men (29 +/- 5 pg/ml). Peak plasma levels were reached during handgrip. E values in men (139 +/- 27 pg/ml) exceeded those in lean women (71 +/- 9 pg/ml; P less than 0.05), and both were higher than the E response in obese women (38 +/- 7 pg/ml; P less than 0.01). While peak plasma NE levels in lean women (654 +/- 62 pg/ml) and obese women (524 +/- 46 pg/ml) were comparable, both were significantly lower than the NE response in lean men (1014 +/- 114 pg/ml; P less than 0.02). Increments in plasma FFA during handgrip were 21% and 28% above values during standing (P less than 0.005) in lean men and lean women, respectively, whereas no net increment occurred in obese women. The excursion of plasma beta-hydroxybutyrate in recovery was 59% above the standing concentration for lean women (P less than 0.05), but no net increments were observed in obese women or lean men. We conclude that obesity in women is attended by suppressed plasma E responses to isometric exercise, which may explain subnormal excursions of plasma FFA and beta-hydroxybutyrate during handgrip and recovery, respectively. Lean men have greater plasma elevations of E and NE during isometric exertion than women, suggesting an influence of sex on plasma catecholamine regulation.
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PMID:Influence of sex and obesity on plasma catecholamine response to isometric exercise. 710 15


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