Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The results of 2 studies to determine the relationship between hormonal contraceptive (h.c.) use, hypertension, and nephritis are reported. 828 women, 16-50 years of age, were divided into 3 groups. 1 group had never used h.c.s., 1 group was presently using h.c.s., and 1 group had used h.c.s. for the last time more than a year prior to the study. Women 26-35 years of age who were using h.c.s. at the time of the study more often developed hypertension than other groups. The h.c. users who developed hypertension more often had a family history of hypertension or diabetes mellitus, more often had diabetes themselves, and more often suffered from preeclampsia or eclampsia during pregnancy. In a second study, ethinyl estradiol, norethisterone acetate, epsilon aminocapronic acid, desoxycorticosterone acetate, and table salt were administered singly or in combinations to 2 groups of rats. In one group, a Goldblatt-type hypertension was induced with a clamp on the nephric artery. No increase in blood pressure was observed in animals which received only an estrogenic or progestagenic agent. Significant increases in blood pressure were observed in animals that were given combinations of estrogenic and progestagenic agents, however. Significantly increased plasma-resin activity was observed in all animals which were given estrogen, while animals receiving desoxycorticosterone acetate showed a highly significant decrease in plasma-renin activity.
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PMID:[Oral contraceptives, hypertension and nephrosclerosis]. 62 80

We have measured fatty acid synthesis (estimated by incorporation of [1-14C] acetate by tissue slices) by 3 transplantable Morris hepatomas of different growth rates--9618A, 7794A and 5123C--in response to fasting and alloxan-diabetes. Fasting did not alter fatty acid synthesis by the 3 hepatomas, bringing to 5 the number of tumors not tested and found similarly insensitive. Diabetes caused reduced fatty acid synthesis in 7794A and 5123C but not by 9618A. Host liver fatty acid synthesis was influenced by the presence of the tumor.
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PMID:The lack of effect of fasting and alloxan-diabetes on the rate of fatty acid synthesis by some Morris hepatomas. 68 81

A parameter of peripheral insulin activity (A = 10(4)/IpGp) can be obtained after oral glucose loading by simple calcuation using insulin and glucose levels at the glucose peak. In combination with a glucose-independent parameter of beta-cell function (CIR = 100. I/G(G-70) a parameter of glucose tolerance (GT = A-CIR) is defined. The parameters allow one to separate the contributions of beta-cell function and peripheral insulin resistance to the glucose tolerance observed after glucose loading. Examples, based on the literature and our own work, illustrate the increase of A and GT by cortisone acetate premedication as well as long-term oral contraceptive medication.
Diabetes 1976 Apr
PMID:Glucose tolerance and insulin release, a mathematical approach. II. Approximation of the peripheral insulin resistance after oral glucose loading. 77 22

For the past 4 years this author has treated almost 300 patients with Megace (megestrol acetate) for periods ranging from 6 weeks to 18 months and, in a few instances, longer. Most of the patients received Megace alone, with the remaining group receiving it in combination with 4 other compounds. The development of diabetes mellitus as described in the paper by J.C. Bottino and C.K. Tashima was not observed in any patients. The majority of patients had SMA 12/60 profiles at 6-week intervals during the 1st several months on therapy and later at about 2-month intervals including blood sugars. The several patients who had controlled adult diabetes when placed on Megace therapy alone or in combination developed no exacerbation of their diabetes while on this steroid. All of the patients received 40 mg 4 times daily throughout the period they were on Megace. It is this author's opinion that in the case described by Bottino and Tashima the development of diabetes mellitus was simply coincidental. This opinion is based on the treatment of a large number of patients with this compound.
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PMID:Megace and no diabetes mellitus. 84 8

The effect of ethanol on stimulus-induced insulin secretion was studied, and possible mechanisms were examined in fasting unanesthetized and unrestrained rats with indwelling jugular and aortic catheters. Glucose (150 mg.) or tolbutamide (10 mg.) was given rapidly, i.v., one hour after agavage of ethanol or saline (control). Acutely, ethanol treatment caused marked inhibition of glucose-induced insulin secretion and impaired glucose disappearance rate. Tolbutamide-induced insulin secretion was also significantly inhibited, and decline in glucose was significantly less in ethanol-treated rats. In response to ethanol, serum calcium concentration significantly declined for two hours. In another study, an ethanol metabolite, acetate (0.4 micronmole/min.) or vehicle (control) was infused for 60 minutes prior to 150 mg. glucose pulse. Acetate priming significantly potentiated glucose-induced insulin secretion and also improved glucose tolerance. It is proposed that (1) ethanol in vivo acutely induces hypocalcemia, which inhibits glucose- and tolbutamide-induced insulin secretion--which, in turn, causes glucose intolerance and prevents tolbutamide-induced hypoglycemia. (2)Acetate might be the actual petentiating influence on glucose-induced insulin secretion observed several hours after ethanol treatment.
Diabetes 1977 Apr
PMID:Effect of ethanol on stimulus-induced insulin secretion and glucose tolerance. A study of mechanisms. 84 8

The smooth muscle cell plays an important role in the process of atherogenesis, proliferating in the arterial intima and becoming filled with lipid during the course of the disease. In these experiments the effect of insulin and glucose on sterol synthesis in cultured rat arterial smooth muscle cells was studied. Arterial smooth muscle cells were cultured from pieces of intima and inner media of young rat aortas. The cells were grown in Petri dishes in culture medium with foetal calf serum and when confluent were exposed to insulin or glucose for 24 hours. Insulin in concentrations of 10 micromicron-100 millimicron per ml stimulated the incorporation of sodium [2-(14)C]acetate into non-saponifiable lipids and digitonin precipitable sterols. However, insulin had no effect on the incorporation of labelled mevalonate into cell sterols. Increasing concentrations of glucose in the medium up to 140 mM had had no effect on the incorporation of isotope into sterols, but higher concentrations of glucose caused cell damage and sterol synthesis was markedly depressed. These results may have relevance to the development of atherosclerosis in diabetes and obesity.
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PMID:The effect of insulin and glucose on sterol synthesis in cultured rat arterial smooth muscle cells. 90 24

Diabetes and obesity were noted in 21.3% and 42.3% respectively of 94 patients with adenocarcinoma corporis uteri. Hypertension and ovarian or mammary neoplasia were also common. Obese and diabetic subjects proved more sensitive to treatment with high doses of medroxyprogesterone acetate. Screening for precancerous states or carcinoma of the endometrium in obese and diabetic women is suggested.
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PMID:[Diabetes, obesity and adenocarcinoma of corpus uteri]. 99 85

The recent literature relating to the pathogenesis of diabetic retinopathy, with or without nephropathy, is critically reviewed. Particular attention is given to the (GH) growth hormone hypothesis. The various procedures of hypophysectomy are discussed including the possible ways of suppressing GH production or overproduction by drugs, especially with (MAP) medroxyprogesterone acetate. Personal results obtained with long-term administration of MAP in depot form on alternate days in 10 patients with advanced retinopathy are described. An inconstant and barely significant suppression of the GH response to insulin-induced hypoglycemia was noted in 6 cases showing that a complete pituitary inactivation had not been achieved. Therefore, the modifications observed in the fundus picture seem to have no relationship with such a condition. The features involved were Microaneurysms and Hemorrhages and Exudates. New vessels and retinitis proliterans were unaffected. Subjective improvement in visual acuity appeared to be more frequent with various possible explanations. MAP was without appreciable effect on the clinical and metabolic course of the diabetes or on renal function in cases of concomitant nephropathy. In light of these preliminary results, further investigation seems to be justified. (author's modified) (summary in ENG).
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PMID:[Trial treatment of diabetic retinopathy by inhibition of pituitary somatotropin secretion with MAP]. 112 48

Incorporation of radiolabeled precursors into muscle proteins was studied in isolated rat hemidiaphragms. A mixture of three branched-chain amino acids (0.3 mM each) added to media containing glucose stimulated the incorporation of [14C]lysine into proteins. When tested separately, valine was ineffective, isoleucine was inhibitory, but 0.5 mM leucine increased the specific activity of muscle proteins during incubation with [14C]lysine or [14C]acetate in hemidiaphragms from fed or fasted rats incubated with or without insulin. Preincubation with 0.5 mM leucine increased the specific activity of muscle proteins during a subsequent 30- or 60-min incubation with [14C]lysine or [14C]pyruvate without leucine. Preincubation with other amino acids (glutamate, histidine, methionine, phenylalanine, or tryptophan) did not exert this effect. When hemidiaphragms were incubated with a mixture of amino acids at concentrations found in rat serum and a [14C]lysine tracer, the specific activity of muscle proteins increased when leucine in the medium was raised from 0.1 to 0.5 mM. Experiments with actinomycin D and cycloheximide suggested that neither RNA synthesis nor protein synthesis are required for the initiation of the leucine effect. Leucine was not effective when added after 1 h preincubation without leucine. The concentration of lysine in the tissue water of diaphragms decreased during incubation with 0.5 mM leucine in the presence or absence of cycloheximide, suggesting that leucine inhibited protein degradation. During incubation with [3h]tyrosine (0.35 mM) the addition of 0.5 mM leucine increased the specific activity of muscle proteins, while the specific activity of intracellular tyrosine remained constant and its concentration decreased, suggesting that leucine also promoted protein synthesis. The concentration of leucine in muscle cells or a compartment thereof may play a role in regulating the turnover of muscle proteins and influence the transition to negative nitrogen balance during fasting, uncontrolled diabetes, and the posttraumatic state. Leucine may play a pivotal role in the protein-sparing effect of amino aicds.
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PMID:Leucine. A possible regulator of protein turnover in muscle. 123 98

Two trials were to study alloxan diabetes in goats. The data were grouped: 1) normal fed goats (10); 2) 48-h fasted goats (5); 3) fed goats sampled 96 h after alloxan treatment (5); and 4) goats treated with alloxan following a 48-h fast and sampled 96 h after alloxan treatment with continued fasting (3). Groups 1 and 4 exhibited the following means: serum insulin 43.9, 16.4, 9.4, and 6.7 muU/ml; blood glucose 55.0, 47.3, 219.6, and 485.6 mg/100 ml; blood ketones 4.3, 2.6, 36.6, and 28.6 mg/100 ml; blood acetate 4.7, 4.0, 42.7, and 4.9 mg/100 ml; plasma-free fatty acids 1.8, 10.0, 14.4, and 40.5 mg/100 ml; and plasma triglyceride 13.3, 7.0, 47.6, and 12.2 mg/100 ml. Liver samples from five fed goats before and 12 days after alloxan treatment exhibited the following means: phospholipid 27.5 and 26.1 mg/g; triglyceride 21.2 and 98.9 mg/g; and percent lipid 7.2 and 14.4. The diabetes was accompanied by fatty liver development and probably reduction in utilization of acetate and triglyceride in the fed animals.
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PMID:Blood and liver metabolites in fed and fasted diabetic goats. 124 92


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