Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

All patients examined [52] with malignant disease of the female genital tract showed lymphocyte reactions to encephalitogenic factor (EF) of more than 10% as measured by the macrophage electrophoretic mobility (MEM) test and its modification (MOD-MEM). Whilst 13 patients with non-malignant disease of the genital tract and 30 normals showed lymphocyte reaction to EF of less than 6%, 4 patients with nonmalignant gynaecological disease gave values above the 10% limit. The lymphocyte reactions of this latter group of patients were discussed with respect to their previous clinical histories. Some of the malignant cases were carcinoma of the cervix in situ so that the MEM test would appear to be of value in the early diagnosis of cancer. The need for caution in the interpretation of results is discussed as well as further possible applications of the technique.
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PMID:Macrophage electrophoretic mobility (MEM) test in malignant gynaecological diseases. 77 34

We have investigated, with and without the influence of X-inactivation, the relationship between autosomal gene-dosage and gene-product in a mammalian system, the mouse. The gene was mitochondrial malic enzyme (Mod-2), shown to lie on Chromosome 7 between the albino (c) and shaker-1 (sh-1) loci, and the enzyme was its product, mitochondrial malic enzyme (MOD-2). Gene duplication, with and without the influence of X-inactivation, was achieved using a translocation that involves the insertion of a portion of Chr 7, including Mod-2, into the X, T(X;7)1Ct. A 1:1 relationship for Mod-2 dosage and MOD-2 activity was found in heart mitochondria. Evidence of X-inactivation of Mod-2 was noted in heart and kidney preparations from females carrying a Mod-2 duplication (one copy of Mod-2 in the X and two copies of Mod-2 on Chr 7). We conclude that the expression of an autosomal locus attached to X-chromatin depends upon whether the translocation is in a balanced or unbalanced state.
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PMID:Influence of gene duplication and X-inactivation on mouse mitochondrial malic enzyme activity and electrophoretic patterns. 86 37

Minimal explicit consensus criteria in the management of patients with four indicator conditions were established by an ad hoc committee of primary care physicians practicing in different locations. These criteria were then applied to the practices of primary care physicians located in a single community by abstracting medical records and obtaining questionnaire data about patients with the indicator conditions. A standardized management score for each physician was used as the dependent variable in stepwise regression analysis with physician/practice and patient/disease characteristics as the candidate independent variables. For all physicians combined, the mean management scores were high, ranging from .78 to .93 for the four conditions. For two of the conditions, care of the normal infant and pregnant woman, the management scores were better for pediatricians and obstetricians respectively than for family physicians. For the other two conditions, adult onset diabetes and congestive heart failure, there were no differences between the management scores of family physicians and internists. Patient/disease characteristics did not contribute significantly to explaining the variation in the standardized management scores.
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PMID:Physician management in primary care. 100 13

We have used a continuous intravenous infusion of glucose (6 mg/kg/min), insulin (80 mU/min), epinephrine (6 mug/min), and propranolol (0.08 mg/min) to directly assess insulin resistance in 14 untreated adult onset diabetics with a mean (plus or minus SE) fasting plasma glucose level of 217 plus or minus 17 mg/100 ml. During the infusion endogenous insulin secretion is inhibited and steady-state plasma glucose and insulin levels are achieved after 90 min. Since similar steady-state levels of plasma insulin are achieved in all subjects, the plasma glucose concentration observed during the steady-state period is a measure of an individual's insulin resistance. Under these conditions, the mean (plus or minus SE) steady-state plasma glucose level of the 14 diabetic patients was 350 plus or minus 16 mg/100 ml, while that of 12 normal subjects was 121 plus or minus 4 mg/100 ml. Additional studies were performed in which control subjects and patients with diabetes had their fasting plasma glucose levels acutely raised or lowered to comparable levels before receiving the basic infusion mixture of glucose, insulin, epinephrine, and propranolol. The results of these studies indicated that differences in initial plasma glucose levels could not account for the different glucose responses of the two groups to the basic infusion. Finally, the mean (plus or minus SE) steady-state plasma glucose level of 104 plus or minus 17 mg/100 ml observed during the same basic infusion in five patients with fasting hyperglycemia (mean plus or minus SE, 142 plus or minus 12 mg/100 ml) secondary to chronic pancreatitis suggested that neither chronic hyperglycemia nor hypoinsulinemia per se necessarily lead to insulin resistance. These results demonstrate that marked insulin resistance exists in adult onset diabetics with fasting hyperglycemia. Since previous studies have documented the presence of insulin resistance in patients with chemical diabetes, the possibility exists that insulin resistance may be characteristic of adult onset diabetes mellitus.
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PMID:Demonstration of insulin resistance in untreated adult onset diabetic subjects with fasting hyperglycemia. 111 64

1. In 161 consecutive cases of fluctuant hearing loss and 13 control cases of other causes of deafness, patients were examined for their ability to metabolize a 100 gm. oral dose of glucose. 2. The plasma glucose level in response to the oral dose of glucose was measured at hourly intervals for three hours. 3. Insulin and proinsulin levels were measured in 46 cases of fluctuant hearing loss and in 13 control cases. 4. None of the control group showed borderline or diabetic tolerance curves. 5. Fourteen per cent of the patients with fluctuant hearing loss had borderline glucose intolerance curves and 19 per cent showed diabetic glucose tolerance curves. 6. In patients whose insulin and proinsulin levels were determined, the insulin response to an oral glucose load was typical of adult onset diabetes, i.e., delayed hyperinsulinemia with concomitant hyperglycemia. The hyperinsulinemia was not associated with hyperproinsulinemia. 7. We conclude that in patients with fluctuant hearing loss there is a significantly higher incidence of borderline or diabetic glucose tolerance than in the "control deafness" or "normal population" group.
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PMID:Diabetes mellitus in fluctuant hearing loss. 115 1

A defect in the early phase of insulin secretion has been proposed as a major determinant of the impaired glucose homeostasis of adult onset diabetes. Since the process of aging is also associated with a deterioration of glucose tolerance, we have measured the acute phase of insulin secretion and glucose disposal rate (KG) after a 20 g glucose pulse in 11 normal, healthy men greater than 65 yr and compared it with the response in 11 nondiabetic men 20-31 yr. The mean fasting plasma sugar levels of the aged subjects (107 mg/dl), tended to be higher than that of the young (94 mg/dl). Comparison of Kg provided clear separation (P less than 0.01) of the old (mean Kg = 0.93) from the young population (mean Kg = 1.95). The acute insulin response to the glucose pulse when expressed either as the area above basal for the 10 min post stimulation or as the mean encremental increase above basal at 3, 4 and 5 min (delta 3-5 IRI) was the same in both timing and magnitude for the old and young subjects. Although our aged subjects had clearly abnormal kg's their acute phase of insulin secretion in response to glucose was normal. Seven noninsulin requiring diabetics with fasting plasma glucose levels greater than 140 mg/dl similarly studied had abnormal kg's (mean = 0.55) but markedly attenuated early release of insulin. Therefore, even though in the diabetics a deficiency of acute phase insulin secretion may have contributed to their impaired kg, in our aged subjects the lack of correlation between kg and a deficiency of acute phase insulin release suggests that factors other than an impairment in the early phase of insulin secretion are responsible for their glucose intolerance or, that there is a dissociation between the biologic and immunologic activity of insulin in these aged subjects.
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PMID:Acute-phase insulin secretion and glucose tolerance in young and aged normal men and diabetic patients. 115 58

A 25-year-old obese woman with adult onset diabetes, with known insulin allergy, was evaluated for her insulin response to glucagon. Intravenous injection of glucagon produced severe generlaized allergic reaction. Skin tests with various insulin and glucagon preparations showed allergic reaction to be most pronounced with beef regular single peak and single component insulin, pork regular single peak, beef lente single peak, and neutral regular (beef-pork) single peak insulin. Allergic reactions to numerous glucagon preparations were found to be directly proportional to the amount of insulin contamination in those preparations. Purification of one glucagon lot by column chromatography verified the presence of proinsulin and insulin contaminants in the preparation.
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PMID:Allergic response to glucagon injection as a result of insulin contamination. 118 21

1 In 4058 diabetics, an inverse relation (negative semilogarithmic correlation) was found between the age of onset and the familial aggregation of diabetes mellitus (P less than 0.01). Hence, juvenile (especially infantile) diabetes appears to be predominantly caused by genetic defects (mutations), whereas adult onset diabetes appears to be essentially based on epigenetic factors. 2. In 3890 diabetics with an onset age of more than 10 years, a highly significant predominance of familial diabetes aggregation was observed on the maternal side as compared to the paternal side (P less than 0.001). This finding suggests the possibility of an epigenetic ("teratogenetic") mode of diabetes transmission mediated by the mother.
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PMID:On possible genetic and epigenetic modes of diabetes transmission. 124 72

We investigated a family in which at least 4 men in 3 generations had a syndrome of obesity, mild mental retardation, delayed puberty, macroorchidism, acanthosis nigricans, hyperinsulinemia, and later overt insulin-resistant diabetes mellitus (non-insulin-dependent diabetes mellitus, NIDDM). The patients have markedly curly scalp hair, deficient face and body hair. Their teeth were healthy and normal in size and position. The clinical and biochemical findings and characteristics of the insulin receptors investigated in fibroblasts are reported. There was normal insulin binding to fibroblasts in the 2 brothers and their father. However, insulin-stimulated RNA synthesis was decreased as compared to that of normal control individuals. These findings suggest a postbinding defect of insulin action. The pedigree documents an autosomal dominant mode of inheritance. The diagnosis is of practical importance since it enables medical supervision of gene carriers in a preclinical state of atherosclerotic complications and overt diabetes. The findings in this family have relevance also to the explanation of familial mild mental retardation and to the study of different forms of insulin resistance due to a disturbance in biosignal transfer.
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PMID:Autosomal dominant insulin resistance syndrome due to postbinding defect. 128 80

Diabetes mellitus is commonly associated with systolic and diastolic hypertension, and a wealth of epidemiological data suggest that this association is independent of age and obesity. Much evidence indicates that the link between diabetes and essential hypertension is hyperinsulinemia. Thus, when hypertensive patients, whether obese or of normal body weight, are compared with age- and weight-matched normotensive controls, a heightened plasma insulin response to a glucose challenge is found consistently. A state of cellular resistance to insulin action subtends the observed hyperinsulinism. Using the insulin/glucose clamp technique in combination with tracer glucose infusion and indirect calorimetry, it has been demonstrated that the insulin resistance of essential hypertension is located in peripheral tissues (muscle), is limited to nonoxidative pathways of glucose disposal (glycogen synthesis), and correlates directly with the severity of hypertension. The reasons for the association of insulin resistance and essential hypertension can be sought in at least four general types of mechanisms: sodium retention, sympathetic nervous system overactivity, disturbed membrane ion transport, and proliferation of vascular smooth-muscle cells. Physiological maneuvers, such as caloric restriction (in the overweight patient) and regular physical exercise, can improve tissue sensitivity to insulin; good evidence indicates that these maneuvers also can lower blood pressure in both normotensive and hypertensive individuals. Insulin resistance and hyperinsulinemia also are associated with an atherogenic plasma lipid profile. Elevated plasma insulin concentrations enhance very-low-density lipoprotein (VLDL) synthesis, leading to hypertriglyceridemia. Progressive elimination of lipid and apolipoproteins from the VLDL particle leads to an increased formation of intermediate density and low-density lipoproteins, both of which are atherogenic. Last, insulin per se, independent of its effects on blood pressure and plasma lipids, is known to be atherogenic. The hormone enhances cholesterol transport into arteriolar smooth-muscle cells and increases endogenous lipid synthesis by these cells. Insulin also stimulates the proliferation of arteriolar smooth-muscle cells, augments collagen synthesis in the vascular wall, increases the formation of and decreases the regression of lipid plaques, and stimulates the production of a variety of growth factors. In summary, insulin resistance appears to be a syndrome that is associated with a clustering of metabolic disorders, including type II diabetes mellitus, obesity, hypertension, lipid abnormalities, and atherosclerotic cardiovascular disease.
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PMID:Insulin resistance, hyperinsulinemia, and coronary artery disease: a complex metabolic web. 128 37


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