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Query: UMLS:C0011860 (type 2 diabetes)
57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Non-insulin-dependent diabetes mellitus patients are those patients who do not require insulin for survival and do not have gestational, secondary, or malnutrition-related diabetes. They may require insulin to maintain good health. Therapy in NIDDM should attempt to reverse the coexisting defects of insulin deficiency and insulin resistance that lead to hepatic glucose over-production and diminished glucose tissue utilization. Both sulfonylureas and insulin can achieve near normal FPGs and HbA1c concentrations in mild to moderately severe NIDDM. Both can reduce insulin resistance and both increase insulin availability. Evidence exists, however, showing that prevention of post-prandial hyperglycemia, whose significance is unknown, may require soluble preprandial insulin. Treatment goals should be realistic and discussed with the patient. In younger patients, the aim should be to achieve normoglycemia, while in those who have other significant medical or social problems, or who are of advanced age, diabetic control may, out of necessity, need to be relaxed. At presentation a diet and exercise program should be initiated and the patient observed if clinically well. If diet fails to reduce the FPG below 108 mg/dl, additional therapy should be used. In mild to moderate NIDDM, sulfonylurea or basal insulin (given as once daily long- or intermediate-acting insulin) can be equally successful without the need for rigid dietary habits. More severe degrees of NIDDM or patients with sulfonylurea failure not caused by dietary indiscretion will require more complex insulin regimens. The socially dependent patient requiring insulin should have as simple a regimen as possible. The insulin-resistant patient undergoing surgery or with an intercurrent illness is most easily managed with a variable rate insulin infusion that allows prediction of subsequent subcutaneous insulin requirements. Combination insulin-sulfonylurea therapy should be reserved for patients failing to achieve acceptable glycemic control when insulin and sulphonylurea are used separately. It may improve control or lessen insulin requirements.
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PMID:Insulin: either alone or combined with oral hypoglycemic agents. 305 69

Despite reports of reduced serum insulin-like growth factor (IGF) levels in experimentally diabetic animals, human diabetic patients have been reported to have decreased, normal, or even elevated levels. This study was a cross-sectional examination of the effect of age on immunoreactive IGF-I levels in adult patients with insulin-dependent or noninsulin-dependent diabetes mellitus (IDDM and NIDDM) attending a diabetes out-patient clinic. The patients and normal subjects studied were divided into the age ranges 21-30, 31-40, 41-50, 51-60, and over 60 yr. For all ages combined, the mean IGF-I level (+/- SD) was 0.84 +/- 0.26 U/ml (202 +/- 62 ng/ml) in 133 normal subjects, significantly reduced to 0.41 +/- 0.17 U/ml in 121 IDDM patients, and 0.49 +/- 0.19 U/ml in 46 NIDDM patients (both P less than 0.001). In both groups there was a marked decline in IGF-I with increasing age (P less than 0.01). Except for NIDDM patients aged 21-30 yr (only two patients), IGF-I levels in both IDDM and NIDDM patients were significantly lower in every age range than those in age-matched normal subjects, but did not differ between the two diabetic groups. Glycosylated hemoglobin levels correlated inversely with IGF-I levels only in younger patients with IDDM (r = -0.486; P less than 0.05 for patients aged 21-40 yr). We conclude that factors common to IDDM and NIDDM, perhaps related to relative nutritional deficiency at the cellular level, cause a reduction in serum IGF-I levels, and that this reduction occurs independently of age-related changes in IGF-I.
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PMID:Serum insulin-like growth factor I levels in adult diabetic patients: the effect of age. 373 35

Individuals with tropical pancreatic diabetes (TPD) have features of malnutrition and insulin-dependent diabetes but do not exhibit ketosis on withdrawal of insulin. Fasting and postglucose C-peptide responses were assessed in TPD and compared with noninsulin-dependent (NIDDM), insulin-dependent (IDDM), and control groups, matched for body weight. The C-peptide concentrations were lower in TPD in comparison with the controls and NIDDM patients but were significantly higher than in classical IDDM. It is likely that the higher C-peptide is responsible for the ketosis resistance in these patients.
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PMID:Pancreatic beta-cell function in tropical pancreatic diabetes. 635 77

Systematic studies of diabetes prevalence and incidence are now indicating the extent and impact of the disease and its complications. A major handicap in establishing a true global picture has been the lack of uniformity in defining and classifying diabetes, and an additional limiting factor has been the grouping of different types of diabetes in published prevalence data. It appears the prevalence of insulin dependent (Type 1) and non-insulin dependent (Type 2) diabetes varies between and within ethnic groups, e.g. rural versus urban dwellers, thus making it difficult to compare data from different countries. However, this fact provides unique opportunities to study the relative importance of genetic and environmental factors in the aetiology of diabetes and its micro- and macrovascular complications. Probably the most urgent needs have been the standardization of classification and criteria, and of epidemiological methodology. This paper will cover the epidemiology of diabetes in terms of the new WHO classification: Insulin dependent diabetes mellitus = Type 1. Non-insulin dependent diabetes mellitus = Type 2. Other types, e.g. pancreatic or tropical malnutrition, endocrine, drug induced, etc. The main forms of diabetes seen in developed countries are Types 1 and 2. They appear to be two distinct clinical entities, but the concept of genetic-environmental interaction in their causation is probably equally applicable. In developing countries, Type 2 diabetes appears to be the most common form, but tropical malnutrition diabetes also occurs in many regions of the globe.
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PMID:The global epidemiology of diabetes mellitus. 668 May 14

Because the supplementation of pyridoxine (vitamin B6) improves the glucose tolerance in gestational diabetes and adult onset diabetes, pyridoxine deficiency has been considered to be one of the factors that cause diabetes mellitus. We produced pyridoxine deficient rats by giving pyridoxine-free food with deoxypyridoxine which competitively the activity of pyridoxal phosphate. In these pyridoxine deficient rats plasma insulin during the glucose tolerance test was significantly low as compared with controls. In vitro experiments of pancreas perfusion showed that secretion of insulin and glucagon was impaired in the pyridoxine deficiency. Since the restriction of diet-calorie caused a decrease in arginine-induced secretion of insulin and glucagon from the isolated pancreas, the impairment of the endocrine pancreas may depend on malnutrition. Pyridoxine deficiency is surely one of the factors that impair the endocrine pancreas by multifactorial derangement of metabolism besides the tryptophan-nicotinic acid pathway.
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PMID:The endocrine pancreas in pyridoxine deficient rats. 703 87

Fifty-seven patients of non-insulin dependent diabetes mellitus (NIDDM) were divided into various groups by Syndrome Differentiation in TCM and 18 cases of non-diabetes mellitus were taken as control. The relationship of Syndrome-types and defect of the erythrocyte insulin receptors were studied with the percentage of specific insulin binding to erythrocyte, number and average affinity of erythrocyte insulin receptors. The results showed: (1) The patients of NIDDM had defect of erythrocyte insulin receptors specified with decreased number of insulin receptors; (2)Mild defect of erythrocyte insulin receptors was found in Syndrome of Yin Deficiency and hyperactivity of Heat, but serious defect in the Syndrome of both Qi and Yin Deficiency, in the Syndrome of both Yin and Yang Deficiency. Above data suggested that the defect of erythrocyte insulin receptors was correlated with Syndrome-types of patients with NIDDM, the more serious Deficiency Syndrome, the more serious defect of erythrocyte insulin receptors.
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PMID:[Relationship between various syndrome-types and defect of erythrocyte insulin receptors in non-insulin dependent diabetes mellitus]. 764 Apr 96

The relationship between brain function and syndrome-types of TCM in 51 patients with non-insulin dependent diabetes mellitus (NIDDM) was observed. The syndromes were divided into three types. (1) Yin Deficiency with internal excessive Heat (YDIEH), 15 cases; (2) Qi-Yin Deficiency (QYD), 21 cases; (3) Deficiency of both Yin and Yang (DYY), 15 cases. The control group consisted of 30 healthy subjects matched in age, sex and educational level. The brain function were tested by neurobehavioral and neuroelectrophysiological tests. The former included short-term memory, thinking, eye-hand coordination and emotion tests; the latter consisted of brainstem auditory evoked potentials (BAEP), visual evoked potentials (VEP) and somatosensory evoked potentials (SEP). The results showed that the brain function in YDIEH group approached normal controls, and the brain function in QYD and QYY groups were significantly deteriorated. The results suggested that the brain function were correlated with the syndrome-types of patients with NIDDM. This would be valuable for diagnosis and treatment of NIDDM in TCM.
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PMID:[Study on relationship between brain function and syndrome differentiation-typing of TCM in non-insulin dependent diabetes mellitus]. 784 50

We studies 151 case of diabetes in the young (age at first visit < or = 35 yrs) from January 1982 to June 1990. We classified the 151 cases into non-insulin dependent diabetes mellitus (NIDDM) (38.4%), malnutrition-related diabetes mellitus (MRDM) (36.4%), insulin-dependent diabetes mellitus (IDDM) (9.9%), secondary diabetes mellitus (2.6%) and unclassified category (12.6%). MRDM can be further classified into 2 groups: 22.5 per cent were fibrocalculous pancreatic diabetes (FCPD) and 13.9 per cent were protein deficient pancreatic diabetes (PDPD). Abdominal roentgenography were performed in 103 cases (68.2%) and pancreatic calcification were found in 34/103 (33%). Farming occupation (p = 0.001), abdominal pain (p = 0.005), male sex (p = 0.0015) and cataracts (p = 0.02) were statistically more common in MRDM comparing to NIDDM and IDDM taken together. There were no statistically significant differences in history of alcohol consumption and raw cassava intake between both groups. Family history of diabetes mellitus were more common in NIDDM comparing to IDDM and MRDM.
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PMID:Diabetes mellitus in the young in Srinagarind Hospital. 800 54

Ageing constitutes a risk factor for magnesium deficit. Primary magnesium deficit originates from two aetiological mechanisms: deficiency and depletion. Primary magnesium deficiency is due to insufficient magnesium intake. Dietary amounts of magnesium are marginal in the whole population whatever the age. Nutritional deficiencies are more pronounced in institutionalized than in free-living ageing groups. Primary magnesium depletion is due to dysregulation of factors controlling magnesium status: intestinal magnesium hypoabsorption, reduced magnesium bone uptake and mobilization, sometimes urinary leakage, hyperadrenoglucocorticism by decreased adaptability to stress, insulin resistance and adrenergic hyporeceptivity. Secondary magnesium deficit in ageing largely results from various pathologies and treatments common to elderly persons, i.e., non-insulin dependent diabetes mellitus and use of hypermagnesuric diuretics. Magnesium deficit may participate in the clinical pattern of ageing, particularly in neuromuscular, cardiovascular and renal symptomatologies. The consequences of hyperadrenoglucocorticism-the simplest marker of which is non-response to the dexamethasone suppression test-may include immunosuppression, muscle atrophy, centralization of fat mass, osteoporosis, hyperglycaemia, hyperlipidaemia, atherosclerosis, and disturbances of mood and mental performance through accelerated hippocampal ageing particularly. It seems very important to point out that magnesium deficit and stress aggravate each other in a true 'pathogenic vicious circle', particularly in the stressful state of ageing. The importance of magnesium deficit in the aetiologies of insulin resistance, and the adrenergic, osseous, oncogenic, immune and oxidant disturbances of ageing is still uncertain. Oral physiological magnesium supplementation (5 mg Mg/kg/d) is the best diagnostic tool for establishing the importance of magnesium deficiency. Too few open and double blind studies on the effects of the treatment of magnesium deficiency and of magnesium depletion in geriatric populations have been done. Further study is necessary to assess the true place of magnesium deficit in the pathophysiology of ageing.
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PMID:Magnesium and ageing. II. Clinical data: aetiological mechanisms and pathophysiological consequences of magnesium deficit in the elderly. 815 90

Several endocrine insufficiencies develop with aging. These not only include the sex steroid hormones in both sexes, but probably also growth hormone. These hormonal systems apparently interact at central and peripheral levels. Deficiencies seem to result in altered body composition, with more body fat, particularly in central depots, combined with a decreased muscle mass. In addition, risk factors for cardiovascular disease and non-insulin dependent diabetes mellitus accumulate concomitantly. Intervention studies now begin to show that this is at least partly reversible with appropriate substitution. Nutritional deficiencies with aging may be coupled to these endocrine insufficiencies, perhaps mediated via psychological factors and loss of energy, which are also associated with the body alterations. If these deficiencies can be successfully corrected, then part of the nutritional problem of aging people may well develop into a more organizational, psychosocial and political type of problem.
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PMID:Endocrine insufficiency and nutrition in aging. 839 47


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