Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A novel model of nutritionally induced hypertension in the rat is described. Dietary obesity was produced by providing sweet milk in addition to regular chow, which elicited a 52% increase in caloric intake. Despite 54% greater body weight gain and 139% heavier retroperitoneal fat pads, 120 days of overfeeding failed to increase systolic pressure in the conscious state (125 +/- 8 vs. 121 +/- 4 mmHg in chow-fed controls) or mean arterial pressure under urethan anesthesia (71 +/- 4 vs. 63 +/- 3 mmHg). In contrast, mild hypertension developed in intermittantly fasted obese animals (a 21-mmHg increase in systolic blood pressure measured in the conscious state and a 16-mmHg increase in mean arterial pressure under anesthesia relative to chow-fed controls). The first 4-day supplemented fast was initiated 4 wk after the introduction of sweet milk, when the animals were 47 g overweight relative to chow-fed controls. Thereafter, 4 days of starvation were alternated with 2 wk of refeeding for a total of 4 cycles. A rapid fall in systolic blood pressure (12 +/- 2 mmHg at 2 days) accompanied the onset of supplemented fasting and was maintained thereafter (2.7 +/- 2.6 mmHg further decrease during the latter half of the fast). With refeeding, blood pressure rose precipitously (13 +/- 3 mmHg in the 1st 2 days), despite poststarvation anorexia. Blood pressure tended to rise slightly over the remainder of the realimentation period (5.2 +/- 2.8 mmHg). After the 4th supplemented fast, hypertension was sustained during 30 days of refeeding. Cumulative caloric intake in starved-refed rats fell within 2% of that in chow-fed controls.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Refeeding hypertension in dietary obesity. 333 69

Rat body size and tissue composition changes from pre-weaning to three months age resulted from voluntary hyperphagia triggered by offering a cafeteria diet. The effects of a 24 hour starvation period in both cafeteria and chow fed controls were compared. Obesity develops earlier in females than in males. This difference is related to the growth patterns in both sexes. Obesity occurs at the stages of development when growth rate decreases. Cafeteria fed female rats attained a 32% greater weight than their controls, with lumbar adipose cords that were 4 times heavier and brown interscapular adipose tissue 2 times heavier than controls. The overall cafeteria fed versus chow fed rat differences in the effects of a 24 hour starvation, were minor but less liver glycogen and much more skeletal muscle lipids were mobilized in the cafeteria fed rats than in controls.
 ...
PMID:Body weight and tissue composition in rats made obese by a cafeteria diet. Effect of 24 hours starvation. 339 32

The biological significance of ketonemia of brief duration and moderate proportions during pregnancy remains uncertain. Thus, controversy persists about whether caloric restriction for obese women during pregnancy, particularly when the obesity is complicated by gestational diabetes mellitus (GDM), constitutes appropriate therapy. We have demonstrated, in a rigorously controlled setting using a Clinical Research Center, that all of the features of 'accelerated starvation' become manifest after 14 h and before 18 h of dietary deprivation. Women with GDM exhibit the same capacity for early 'accelerated starvation' as in normal pregnancy; thus, their insulin deficiency and insulin resistance do not appear to be sufficient to render them increasedly at risk for uncontrolled catabolism. Some cautious exploration of the use of hypocaloric diets as a therapeutic approach to the metabolic disturbances of GDM may be justified.
 ...
PMID:Accelerated starvation in pregnancy: implications for dietary treatment of obesity and gestational diabetes mellitus. 355 61

The efforts of the dietitians have lately been directed to elaboration of super low energy diets for the treatment of obese patients. A low energy variant of diet No 8 of Pevzner of 2512.2 kJ (600 kcal) daily has been tried in a group of 66 patients with obesity, degree II and III. The duration of that king of dietary treatment lasted 10-14 days under clinical conditions. A good tolerance to the diet was established in all patients as well as absence of adverse effects. Improvement and abatement of the subjective complaints, associated with the basic disease, were observed. The patients, prior to that dietary variant had been treated with traditional diet No 8 Pevzner with a total course of treatment at the clinic of 20 days. The total mean body reduction attained was 8 kg. The result obtained is relatively better than that with the traditional diet 8 and comes closer to the results attained with the energy-free zero diet. That provided grounds to recommend the low energy variant studied as a more adequate in effectiveness and physiology as compared with the therapeutic starvation, applied so far in the treatment of patients with body mass above the norm.
 ...
PMID:[Therapeutic effect of a low-energy diet in patients with above-normal body weight]. 371 83

Obesity, a well-known phenomenon in Western society, is frequently associated with cardiovascular and endocrine disease. Strokes, myocardial infarction, diabetes and hyperlipidemia are classical reasons for the high mortality and morbidity of overweight people. For this reason, intensive weight-reduction programs have been proposed: low-calorie diets, total starvation, drugs and even surgery. Total starvation and some low-calorie diets are, however, also associated with sudden death, most probably of cardiac origin. Experimental data from our laboratory show that total starvation is accompanied by a severe depletion of magnesium in myocardial tissue. Protein-sparing modified low-calorie diets, however, can protect against this mineral loss even if magnesium supplementation alone cannot obtain this goal. Applying these principles in overweight man show weight reduction without mineral loss or cardiac disturbance. Surgery with 'ileal bypass' procedures gives rise to severe hypomagnesemia and hypocalcemia with tetany and spasmophilia. New procedures, derived from experimental surgery, are 'gastric bypass' and 'gastroplasty'. These methods, only applied in very obese patients (body mass index greater than 40, normal 23-27) show no change in mineral concentrations of calcium and magnesium and no clinical symptoms suggestive for mineral loss. A good, controlled weight-reduction program under strict medical surveillance can, in this way, offer new perspectives in the treatment of one of our most frequent 'culture-induced' diseases.
 ...
PMID:Magnesium and obesity: effects of treatment on magnesium and other parameters. 382 Nov 74

Responses of the hepatic lipogenic enzymes, glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase (6PGDH), and malic enzyme (ME) to starvation refeeding and diet shifting were determined in lean and obese female Zucker rats. Rats were either fed nonpurified diet, starved 48 hr, and then refed nonpurified diet or one of the refined carbohydrate diets containing either glucose, fructose, cornstarch, or sucrose for 72 hr, or shifted from nonpurified diet directly to one of the refined carbohydrate diets for 72 hr. Initial activities were greater in obese than lean rats for all three enzymes studied. Similar to other strains of female rats, lean Zucker rats failed to demonstrate a starve-refeed response when refed nonpurified diet. Obese female littermates showed a statistically significant increase in enzymes when refed a nonpurified diet. Both lean and obese female Zucker rats demonstrated increases in enzyme activities above controls when starved and refed any of the refined carbohydrate diets. The greatest responses were observed when female rats were starved and refed sucrose; activities increased 2.6- to 3.5-fold in lean and 3.0- to 4.3-fold in obese Zuckers. In lean females 50-70% of the starve-refeed response observed with G6PDH and ME can be accounted for by simply shifting from a nonpurified diet to the respective refined carbohydrate diet, whereas in obese females only 33-55% of the increase could be attributed to diet shifting. Plasma testosterone/estrogen ratios were consistently 1.5 times higher in obese than in lean female rats. This phenotypic difference may potentiate the heightened starve-refeed overshoot response observed in obese rats.
 ...
PMID:Dietary induction of hepatic glucose-6-phosphate dehydrogenase, 6-phosphogluconate dehydrogenase, and malic enzyme in lean and obese female Zucker rats. 382 5

We propose a rational regimen for management of non-insulin-dependent pregnant diabetics (NIDD), using appropriately constituted calorie-restricted diets with the oral agents metformin and glibenclamide as may be necessary, with rapid recourse to insulin if the latter do not produce excellent control of blood glucose. Using this regimen between June 1974 and December 1983 we have managed 423 new diabetics (ND, diagnosed during pregnancy) with a perinatal mortality (PNM) of 14 per 1000 and 268 established diabetics (known diabetics, KD) with a PNM of 70/1000 (57/1000 since 1978). A further 80 NIDDs were 'untreated', i.e., not seen by us until near term; these suffered a PNM of 313/1000. Side-effects of the drugs have been few and mild, they are not teratogenic; 'starvation ketosis' does not occur; neonatal hypoglycaemia is preventable by using continuous insulin infusion during delivery. We suggest that the regimen outlined here is acceptable to the patients, is safe, gives excellent results and furthermore teaches the diabetic mother proper dietary control and combats lifelong obesity. It should be useful especially in developing countries in which pregnant, overweight NIDDs are common. Precise control of the blood glucose is essential.
 ...
PMID:The management of non-insulin-dependent diabetes during pregnancy. 393 18

Carnitine metabolism during starvation was studied in adult lean and obese female Zucker rats. Comparisons were made between rats starved for 0, 3, 6 or 9 d. Total plasma carnitine was not affected by obesity or starvation, but free plasma carnitine decreased with starvation. Plasma acid-soluble acylcarnitine was lower in obese than in lean rats, and increased with starvation in both lean and obese rats. Plasma acid-insoluble acylcarnitine was not affected by obesity but increased with starvation. Liver free and acid-soluble acylcarnitine were lower in obese rats than lean rats, and starvation increased liver free carnitine and acid-insoluble acylcarnitine. Free carnitine was lower in muscle from obese rats than from lean rats. In kidney, free carnitine decreased during starvation. Heart carnitine was not affected by obesity or starvation. Urinary free carnitine and acid-soluble acylcarnitine clearance decreased during starvation. These studies indicate that: 1) lean and obese Zucker rats conserve carnitine during starvation; and 2) the decreases in liver carnitine concentration reflect the loss of cellular constituents rather than increases in total hepatic carnitine.
 ...
PMID:Carnitine metabolism in lean and obese Zucker rats during starvation. 395 11

Serum cholesterol concentrations, lecithin-cholesterol acyltransferase (LCAT), and hepatic 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase activities of lean and obese Zucker rats were compared. The excess serum cholesterol of the female obese rat is found to be mainly free cholesterol associated with very low-density lipoproteins, whereas that of the male obese rat is carried as cholesterol esters associated with high-density lipoproteins. The high level of serum free cholesterol in the female obese rat is not due to a deficiency in lecithin-cholesterol acyltransferase activity. This enzyme activity is found to be elevated in the male obese rat. Hepatic HMG-CoA reductase activity declines as rats mature; this observation is most apparent in obese male rats. Lean rats exhibit the normal diurnal rhythm, but mature obese rats show little diurnal variation in HMG-CoA reductase activity. Obese female rats maintain high reductase activities, but the activities of obese male rats remain low at all times. Starvation suppresses liver HMG-CoA reductase and serum cholesterol in both lean and obese female rats. Thus, an increase in hepatic cholesterol synthesis may contribute to hypercholesterolemia in the obese female Zucker rat. On the other hand, factors such as nonhepatic synthesis or a decreased cholesterol catabolism may play more important roles in maintaining high serum cholesterol in the obese male Zucker rat.
 ...
PMID:Serum cholesterol, lecithin-cholesterol acyltransferase, and hepatic hydroxymethylglutaryl coenzyme A reductase activities of lean and obese Zucker rats. 396 58

Unilateral electrolytic lesions of the medial hypothalamus have previously been reported to spare starvation-induced lipid mobilization from the ipsilateral retroperitoneal fat pad. This suggests that deficient lipid mobilization contributes to the enhanced lipid deposition which results when such lesions are bilateral. In contrast, unilateral parasagittal hypothalamic knife cuts, which also obesify when bilateral, failed to prevent starvation-induced ipsilateral lipid mobilization. This finding indicates that impairment of neurally mediated lipid mobilization is probably neither a necessary nor a sufficient feature of hypothalamic obesity.
 ...
PMID:Adipose tissue mobilization is unaffected by obesifying hypothalamic knife cuts. 403 93


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>