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

The lipoprotein-lipase activity (LPLA) in the abdominal, subcutaneous, adipose tissue was studied in a random sample (n = 69) of 60-year-old men. A new method for the quantification of LPLA was applied. The mean value was 67 mU/g when expressed per gram (wet weight) of adipose tissue. Several subjects within the lower part of the range of adipose-tissue LPLA values had low concentrations of serum-triglycerides (S-TG). There was no correlation between the LPLA and S-TG concentrations in the fasting state. Among the 69 subjects, four had newly detected diabetes mellitus and had significantly lower LPLA in the adipose tissue than the control group. The fat-cell size and the LPLA per gram of adipose tissue were not correlated. Thus, obesity without diabetes mellitus does not imply a low LPLA concentration in adipose tissue. The variation of the concentration of adipose-tissue LPLA in the fasting state in this population was explained only to a minor extent by the variation of S-insulin and blood-glucose parameters, when analysed statistically by a stepwise multiple-regression technique.
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PMID:Lipoprotein-lipase activity in subcutaneous, adipose tissue in healthy subjects: variation of activity in a population of 60-year-old men. 3 Jan 95

Short chain fatty acid absorption from the human rectum has been studied in 46 subjects attending an obesity clinic, using a dialysis bag technique. From a mixed electrolyte solution, acetate concentrations fell from 97.0 to 64.2 mmol/l, and sodium from 97.8 to 85.1 mmol/l with respective net absorption rates of 8.1 and 5.2 mumol/cm2/h. From a solution with mixed short chain fatty acids acetate concentration fell from 62.3 to 37.6 mmol/l, propionate from 20.2 to 11.5 mmol/l, and butyrate from 25.7 to 17.3 mmol/l with absorption rates of 5.2, 1.8, and 1.9 mumol/cm2/h. Lowering pH from 7.2 to 5.5, to test the possibility that absorption occurred by passive non-ionic diffusion, had no effect on absorption rates, although pH rose rapidly in the dialysis fluid. These results are comparable with rates of acetate absorption from the animal large intestine. The hypothesis that short chain fatty acids are not absorbed from the large gut and therefore contribute to faecal bulk by retaining water in the bowel lumen may need revision.
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PMID:Short chain fatty acid absorption by the human large intestine. 3 Jun 83

Obesity results when the ingestion of energy exceeds its utilization, leading to an excessive expansion of the adipose tissue mass. Current pharmacological therapy for the obese patient focuses primarily on reducing energy intake. Anorectic agents reduce food consumption by modifying central systems in the brain which are involved in appetite regulation. These agents are reviewed in terms of mechanism of action, and clinical safety and efficacy in suppressing appetite and promoting weight loss. Newer anorectic agents which are being evaluated currently in clinical and animal studies are described. Clinical assessments of therapeutic regimens utilizing the thyroid hormones and human chorionic gonadotropin are evaluated. Finally, an overview of novel pharmacological approaches to the treatment of obesity is presented.
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PMID:Pharmacological treatment of obesity. 3 Jul 32

1. The insulinogenic factor of the gastrointestinal mucosa named "incretin" is only one part of the complex enteroinsular axis. --2. Of the chemically defined gastrointestinal hormones GIP is the strongest incretin candidate. --3. Because of the dual function of GIP as gastrone and insulinotropic substance several safeguards against GIP-mediated insulin hypoglycaemia exist. --4. No pathological condition has yet been found which is causally related to hyper- or hyposecretion of GIP. However, an exaggerated GIP response (usually secondary to the disease) may participate in the pathogenesis of hyperinsulinaemia of patients with obesity and duodenal ulcer. --5. The injection of GIP antibodies only partially abolishes the incretin effect. Therefore, GIP, although important, is not the only incretin.
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PMID:The incretin concept today. 3 19

1 Thirty-three patients with no evidence of endocrine disease, hepatic or renal insufficiency or sleep disorders, were classified in groups 1 to 4 in order of increasing of percentage of ideal body weight (IBW) respectively: less than 90% of IBW, 90--120%, 120--180%, and greater than 180% of IBW. After oral administration of 200 mg butobarbitone, concentration of the intact drug was measured by gas liquid chromatographic assay in urine samples collected during 72 h and at three times in blood. 2 A highly significant negative relationship was found between the cumulative excretion of butobarbitone with urine and the logarithm of the percentage of IBW. In contrast for a given weight, excretion of the drug with urine was found to be weakly correlated with the diuresis. 3 The cumulative urinary elimination of butobarbitone was significantly different between the groups studied, except of the difference between the group 2 and 3 of the patients. No significant difference was found between the renal clearances of butobarbitone in the four groups of subjects. 4 We conclude that redistribution of butobarbitone into adipose tissues can explain the obtained results and that obesity modifies the pharmacokinetics of the drug.
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PMID:Study of urinary excretion of butobarbitone in man in relation to the percentage of ideal body weight. 3 16

1. Rapid effects of hormones on the metabolism of glycogen and fatty acids were studied in the perfused liver of normal and genetically obese (ob/ob) mice. 2. In livers from normal and obese mice adrenaline and angiotensin II stimulated glycogenolysis. 3. These hormones inhibited the synthesis de novo of long-chain fatty acids in livers from normal mice, but not in livers from obese mice. 4. The proportion of acetyl-CoA carboxylase in the active form was decreased by adrenaline but not by angiotensin II in livers from obese mice. 5. The potency of hormone effects on liver suggests that they could occur in the intact animal. 6. The results add to the evidence that hepatic fatty acid synthesis in genetically obese (ob/ob) mice is irreversibly resistant to inhibition by a range of hormones. Such resistance could be of primary significance in the pathogenesis of the obesity.
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PMID:Catabolic effects of adrenaline and angiotensin II in the perfused liver of normal and genetically obese (ob/ob) mice. 3 34

The administration of monosodium-L-glutamate (MSG) during the neonatal period is known to result in central nervous system lesions in the arcuate nucleus of the hypothalamus and the retina. Rodents so treated exhibit behavioral deficts and endocrinopathies including obesity, hypogonadism, hypothyroidism, pituitary atrophy, tail automutilation and diminished locomotor activity. Assessment of endocrine status revealed normal serum levels of glucagon, thyroid-stimulating hormone and luteinizing hormone, and diminished levels of thyroid hormones and growth hormone in MSG-treated rats. Prolactin levels were elevated in the glutamate-treated male rats. Within the brain hypothalamic levels of thyrotropin-releasing hormone, luteinizing hormone-releasing hormone, and somatostatin were unchanged. Measurement of neurotransmitters and neurotransmitter-related enzymes in individual hypothalamic nuclei derived from MSG-treated rats revealed normal levels of norepinephrine, serotonin and glutamic acid decarboxylase, but reduced levels of choline acetyltransferase and dopamine in the arcuate nucleus and median eminence. Histochemical methods for visualization of dopamine and acetylcholinesterase in the mediobasal hypothalamus confirmed these findings. The MSG-treated animals exhibited a normal diurnal rhythm of pineal serotonin N-acetyltransferase activity. These data indicate that the MSG-induced endocrine deficiency syndrome results at least partly from destruction of cholinergic and dopamingeric tuberoinfundibular systems in the hypothalamus.
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PMID:Models of neuroendocrine regulation: use of monosodium glutamate as an investigational tool. 3 35

1. The aim of this investigation was to ascertain of a variety of obese rodents whether the primary cause of fat cell enlargement lay in the fat cell itself, or in its environment. Rodents studied were the mutant mice 'diabetic' (db/db), 'adipose' (dbad/dbad), and 'yellow obese' (Ay/+), New Zealand obese mice, CBA mice made obese with gold thioglucose, and obese BIO 4.24 hamsters. 2. Gonadal fat of obese or lean genotype was transplanted under the kidney capsule of an obese or lean host. Grafts were left in place for at least one month, then examined histologically to measure fat cell diameters, from which fat cell masses were calculated. 3. Immunological rejection of grafts was avoided either by using mice syngeneic except for the obesity producing mutation (db/db, dbad/dbad or Ay/+) or by transplanting into F1 hybrids (NZO X BALB/c) made by mating the strains acting as donors of obese or lean fat. Transplantation of fat between lean BIO 4.22 hamsters and obese BIO 4.24 hamsters was possible because these had common histocompatibility antigens. 4. In all the forms of murine obesity studied, 'lean' fat cells enlarged in an obese recipient to the size typical of cells in 'obese' fat whilst 'obese' fat cells shrunk in a lean recipient to, at least, the size typical of 'lean' fat. Lean hamster fat cells also enlarged in an 'obese' environment and 'obese' hamster cells shrunk in a 'lean' environment. 5. Environment therefore contributes to the determination of fat cell size in all the rodents studied, and in several rodents (db/db, dbad/dbad, Ay/+, and gold thioglucose obese mice) our results showed that environmental factors are of paramount importance in determining cell size, and factors associated with the fat cell itself make a negligible contribution.
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PMID:Is genetically transmitted obesity due to an adipose tissue defect? 4 Dec 55

Post-operative infection is often due to a combination of several factors. A decrease in immune defence processes represents the first factor. This is seen in situations such as malnutrition (undernourishment or obesity), alcoholism, diabetes, neoplasms, infections and old age. It may also be induced by therapy such as immunodepressants, antimitotic chemotherapy, corticosteroids and radiotherapy. Finally, certain antibiotics have been accused of reducing immune defences. The second factor responsible for infection is bacterial flora. Errors such as broad spectrum antibiotic therapy prescribed in the presence of unexplored fever, or changed repeatedly, are responsible for imbalance in the bacterial flora and the acquisition of resistance to antibiotics. These errors firstly increased the prevalence of infections and, secondly their severity and the difficulty of their treatment. The last factor responsible for infection is rupture of the natural barriers formed by the skin and mucosae. This is related on the one hand to surgery itself and, secondly, to the intensive care techniques surrounding the surgical act: venous catheterization above all, but also bladder catheterization, tracheal intubation, etc.
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PMID:[Factors responsible for post-operative infection]. 4 67

The body cholesterol pool increases with decreasing plasma-high-density-lipoprotein (H.D.L.) but is unrelated to the plasma concentrations of total cholesterol and other lipoproteins. This finding supports existing evidence that H.D.L. facilitates the uptake of cholesterol from peripheral tissues and its transport to the liver for catabolism and excretion. Plasma-H.D.L., is reduced in several conditions associated with an increased risk of future ischaemic heart-disease (I.H.D.), namely hypercholesterolaemia, hypertriglyceridaimia, male sex, obesity, and diabetes mellitus, while subjects with existing clinical I.H.D. have lower levels of H.D.L. than healthy subjects within the same community. It is proposed that a reduction of plasma-H.D.L. concentration may accelerate the development of atherosclerosis, and hence I.H.D., by impairing the clearance of cholesterol from the arterial wall.
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PMID:Plasma-high-density-lipoprotein concentration and development of ischaemic heart-disease. 4 38


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