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

There was no significant difference between the assessments by two groups of randomly-selected general practitioners on the effectiveness of the drug treatment for 19 common clinical conditions. The treatment of simple iron deficiency anaemia was considered the most effective and gained the highest consensus. Least effective, but not matched by worst consensus, was the drug treatment for obesity. The most widespread disagreement among the practitioners was for the effectiveness of the drug treatment of gastroenteritis.
J R Coll Gen Pract 1976 Dec
PMID:The assessment by doctors of the effectiveness of drugs. 101 Dec 6

The authors tested the tolerance and therapeutic effect of desopimon preparation (1-p-chlorophenyl-2-aminopropane hydrochloride) in 44 subjects with obesity--I, II and III degree. They found a manifested appetite-inhibiting effect of the medicament in 41 of the patients and slight in two (the treatment was discontinued in a female, due to urticaria). Side effects, similar to those described with phenformin and phenmethrazin derivatives were not established. Body-weight loss is 12,9 kg per subject for a period of a month and a half, and the analysis of the data revealed that the weight loss was entirely on the account of the fatty tissue reduction. Triglyceride diminution was established in serum whereas free fatty acids were increased. After the confrontation of their own data those of some other researchers, the authors recommend desopimon as a suitable additive means in the treatment of simple nutritive (hyperphagic) obesity.
Vutr Boles 1976 Dec
PMID:[Desopimon in the treatment of obesity]. 101 25

Norepinephrine (NE) levels in the hypothalamus and telencephalon of genetically obese mice with the OBOB and DBDB mutations are significantly higher than those of their lean littermates. Obese mice with the viable yellow mutation failed to show this increase. Restricting the diets of OBOB animals to prevent excessive weight gain does not affect NE levels in the hypothalamus, telencephalon or brainstem.
Pharmacol Biochem Behav 1976 Dec
PMID:Effects of food restriction and mutation on central catecholamine levels in genetically obese mice. 102 29

The insulin resistance seen in obesity, which is characterized by elevated basal levels of insulin and an exaggerated insulin response to such stimuli as glucose ingestion, was thought to be related to another common characteristic of obesity--enlargement of the fat cell. Now, recent studies suggest that the enlarged fat cell is not the major source of insulin insensitivity in obesity and may, in fact, be the victim of the insulin-resistant state.
Hosp Pract 1976 Dec
PMID:Insulin resistance in obesity. 102 24

The pathophysiologic considerations support the causal relationship between the secular trend of sugar consumption in industrialized society and the development of prenatal acceleration, which is evident on the basis of epidemiological data. The excessive consumption of sugar and the other quickly absorbed "refined" carbohydrates enhances the hormonogenic effect of food which is also potentiated by the proteins. Together with the caloric overloading, provoked also by the excess in fat, characteristic for the affluent society, the excessive sugar consumption enhances in the pregnant women obesity and "protodiabetes" (PFEIFFER), in the predisposed child the tendency to hyperinsulinism with its consequences. In a prediabetic mother with normal glucose-tolerance the regularly repeated postprandial overfloating of the fetus with maternal glucose changes the feto-maternal hormonal regulation and enhances together with the overloading of substrate, i.e. energy and elements of biosyntheses, the accelerated fetal growth and especially the obesity of the large baby.
Helv Paediatr Acta 1976 Dec
PMID:[Sugar consumption and prenatal acceleration. II. Studies on the etiology and pathophysiology of secular prenatal acceleration]. 103 12

A study was conducted on 7 fertile women (ages 19-44) after end-side jejunoileostomy for obesity. The peak plasma norethindrone (norethisterone) and levonorgestrel (formerly known as d-norgestrel) levels were measured during separate 24-hour norethindrone or levonorgestrel loads using conventional oral contraceptives (OCs). Compared to normal control patients, the intestinal bypass patients had severely reduced mean levels. The levels were 5.0 versus 20.8 ng/ml for norethindrone and the levels were 1.63 versus 4.25 ng/ml for levonorgestrel. Investigation of the patients' sex steroid binding globulin levels showed markedly reduced levels, implying a defective hepatic synthesis of this globulin rather than malabsorption as the most important factor. The data shows a reduced plasma level of OC in patients operated in this way, and OCs cannot be considered safe after intestinal bypass.
JAMA 1976 Dec 20
PMID:Oral contraceptives after intestinal bypass operations. 103 86

To determine the association between the incidence of endometrial cancer and the use of estrogen in menopausal and post-menopausal women, we retrospectively compared 317 patients with adenocarcinoma of the endometrium with an equal number of matched controls having other gynecologic neoplasms; 152 patients used estrogen, as compared to 54 of 317 controls. Thus, the risk of endometrial cancer was 4.5 times greater among women exposed to estrogen therapy. When estrogen use was adjusted for concomitant variables such as obesity, hypertension, diabetes, parity, referral pattern, age at diagnosis, year of diagnosis and other gynecologic neoplasms, the magnitude of the increased relative risk was associated with several of these variables, and was highest in patients without obesity and hypertension. Exogenous estrogen therapy is associated with an increased risk of endometrial carcinoma, but this increased relative risk is less apparent in patients with physiologic characteristics previously associated with an increased risk.
N Engl J Med 1975 Dec 04
PMID:Association of exogenous estrogen and endometrial carcinoma. 118 89

Adipose tissue from twelve normal-weight and ten obese subjects on weight-maintaining diets and nine obese subjects on hypocaloric diets was removed at surgery and incubated in vitro. Basal glucose oxidation correlated significantly (r = 0.68, p less than 0.005) with fat-cell diameter in subjects on weight-maintaining diets. This relationship was significantly altered (p less than 0.02) in subjects on calorie-restricted diets. In tissue from subjects on weight-maintaining diets, physiologic concentrations of insulin (25 muU./ml.) significantly increased glucose incorporation into carbon dioxide (p less than 0.005) and glycogen (p less than 0.001). Maximum insulin-stimulated glucose oxidation (increase over basal) was significantly enhanced (p less than 0.05) in tissue from obese subjects, whereas insulin-mediated glucose incorporation into glycogen was similar in controls and obese subjects on weight-maintaining diets. Insulin-stimulated glucose oxidation was imparied in tissue from subjects on hypocaloric diets although fat-cell diameter was similar to those of obese subjects on weight-maintaining diets. The effect of insulin on glucose incorporation into glycogen in isolated adipocytes was also studied. There was no correlation between insulin-stimulated glycogen synthesis and cell diameter. When cells from the same individual were separated into small and large adipocytes by differential flotation, the insulin effect was similar whether expressed as absolute or per cent increase over basal. These results indicate that in vitro glucose oxidation by adipose tissue, in both the absence and the presence of insulin, is largely determined by dietary factors. This may also be true for insulin-stimulated glycogen synthesis. No evidence is provided for the concept that the enlarged human fat cell of obesity is insensitive to insulin in vitro.
Diabetes 1975 Dec
PMID:Insulin sensitivity of the large human adipocyte in vitro. 119 13

The epidemiological, clinical and instrumental features of cerebral circulatory insufficiency are examined in an assessment of the criteria required for correct diagnosis. The need to refer to both direct and indirect criteria is illustrated in the light of a series of cases. From the 4th decade of life onwards, males are more prone to cerebral arteriosclerosis. Hypertension, diabetes and obesity are significant risk factors. The findings obtained by various methods of examination are critically discussed. Their correct interpretation naturally demands correlation with the clinical data.
Minerva Med 1975 Dec 12
PMID:[Correlation of some instrumental, metabolic and clinical parameters in cerebral atherosclerosis]. 119 42

Insulin, proinsulin and glucagon extracted from lean rat pancreases were studied in radioimmunoassay, radioreceptorassay and bioassay systems. Extracted insulin behaved identically to a rat insulin used as a reference standard in radioimmunoassay. On the basis of its immunoreactivity, extracted insulin was slightly less potent (about 70%) than the rat standard insulin in competing with the binding of 125I-insulin to rat liver membranes (radioreceptorassay) and in stimulating glucose oxidation by rat fat cells (bioassay). Extracted glucagon and a pork glucagon used as a reference standard were indistinguishable in two radioimmunoassay systems for glucagon, in competing with the binding of 125I-glucagon to rat liver membranes (radioreceptorassay) and in stimulating adenylate cyclase in rat liver membranes (bioassay). Genetically obese rats (Zucker, "fatty") were compared to their lean littermates with respect to insulin, proinsulin and glucagon extracted from their pancreases. Proinsulin represented the same proportion of total immunoreactive insulin in both types of rats. In the radioimmunoassays, the radioreceptorassays and the bioassays, insulin, proinsulin and glucagon from obese rats were indistinguishable from insulin, proinsulin and glucagon from lean rats. It is concluded that the pancreatic hormones of obese ("fatty") rats possess the same immunoreactivity and biological potency as those of nonobese rats. This excludes the possibility that some alteration in the biological properties of pancreas insulin and/or glucagon of fatty rats could explain the metabolic abnormalities observed in this type of obesity.
Diabetologia 1975 Dec
PMID:Glucagon and insulin from lean rats and genetically obese fatty rats: studies by radioimmunoassay, radioreceptorassay and bioassay. 120 22


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