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

While the incidence of essential hypertension is not increased in type 1 diabetics, it is about three times as high in type 2 diabetics. Since in 50% of the cases, hypertension is present before the metabolic disorder becomes manifest, an association between the etiologies of the two disturbances was suspected as long as 65 years ago. A new understanding of the significance of insulin resistance and hyperinsulinemia suggests that the two conditions are part of a single metabolic disorder. This is supported by the fact that normal-weight hypertensives can also manifest insulin resistance, and they more often develop a type 2 diabetes mellitus. These facts urge us to re-think our therapeutic approach to hypertension, and to employ, as far as possible, only those substances that have no negative influence on the incidence of the metabolic disorder. With the introduction of ACE-inhibitors capable of improving insulin sensitivity, we now have, for the first time, the possibility of improving the prognosis of the metabolic syndrome. Moreover, their molecular mechanism of action provides initial clues as to the possible etiology of the syndrome.
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PMID:[Essential hypertension and diabetes mellitus]. 218 85

Diabetes mellitus is a chronic metabolic disorder, which can alter the nutritional status of the individual. Some micronutrients, in particular zinc and chromium, have been implicated in the pathogenesis of carbohydrate intolerance. This review evaluates the available published data on the status of 10 mineral elements and seven vitamins in diabetic patients and experimental animal models of diabetes. The role of these micronutrients in insulin secretion and carbohydrate metabolism is discussed in an attempt to determine whether the reported alterations in serum or tissue content of minerals or vitamins contribute to the carbohydrate intolerance of diabetic patients. It is concluded that both Type I and Type II diabetes mellitus can result in changes in certain micronutrients. However, adequately controlled studies to establish the role of trace elements in the pathogenesis of diabetes mellitus are not available.
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PMID:Micronutrient status in diabetes mellitus. 355 60

Non-insulin-dependent diabetes mellitus (NIDDM) is a complex metabolic disorder with a significant genetic component. Obesity is a frequent complicating factor for NIDDM. In the mouse, a number of single gene defects that result in obesity have been described. Mutations in one of these genes, the ob gene, results in both obesity and NIDDM. Recently, the cloning of the murine ob gene and its human homologue has been reported (Nature 372:425-432, 1994). In the present study, the contribution of genetic variation at the human ob locus to NIDDM susceptibility was assessed by analyzing allele sharing in NIDDM-affected sib pairs (ASPs) for markers located near the human ob gene. Four yeast artificial chromosome clones containing the human ob gene were isolated. These clones colocalized the ob gene and two microsatellite markers, D7S514 and D7S635, to a region of 280 kb on the long arm of human chromosome 7. The microsatellite markers were typed in 346 Mexican-American NIDDM-ASPs derived from 176 families and an additional 110 ethnically and geographically matched controls. No evidence of linkage or association between either microsatellite marker and NIDDM was observed in this population. These results suggest genetic variation in the human ob gene does not play a major role in susceptibility to NIDDM in Mexican-Americans.
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PMID:Identification of microsatellite markers near the human ob gene and linkage studies in NIDDM-affected sib pairs. 762 7

Non-insulin-dependent diabetes mellitus is a complex metabolic disorder that involves numerous biochemical abnormalities, a heterogenous clinical picture, and a polygenic hereditary component. The pathophysiologic state involves increased basal hepatic glucose production, decreased insulin-mediated glucose utilization in target tissues, and altered pancreatic function with decreased beta cell function and enhanced glucagon secretion. Prospective studies indicate that insulin resistance and hyperinsulinemia exist in the prediabetic state at a time when glucose tolerance is normal. When hyperglycemia supervenes, both insulin secretion and insulin-mediated glucose utilization are further compromised, mediated in part by sustained hyperglycemia itself. Insulin resistance may occur at any level in the biologic action of insulin, from initial binding to cell surface receptors to the phosphorylation cascade that is initiated by autophosphorylation of the insulin receptor. Receptors isolated from patients with non-insulin-dependent diabetes mellitus have compromised autophosphorylation-kinase activity when isolated from adipocytes, liver, erythrocytes, and skeletal muscle. The magnitude of the decrease in insulin receptor kinase activity is correlated with the degree of fasting hyperglycemia. However, the defect in insulin receptor kinase activity is normalized after weight reduction or other measures that reduce hyperglycemia, indicating the secondary nature of the defect. Clarification of the mechanisms underlying insulin resistance in non-insulin-dependent diabetes mellitus will lead to new treatment modalities for this disease.
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PMID:Insulin resistance and non-insulin-dependent diabetes mellitus: cellular and molecular mechanisms. 790 Jun 97

Diabetes mellitus is a metabolic disorder which has affected several millions of population all over the world. It is characterized by an excess of sugar in the blood and urine, hunger, thirst and gradual loss of weight. Insulin is a hormone which regulates the carbohydrate and triacylglyceride metabolism through its action at several sites and facilitates the entry of glucose accumulation in the blood. Insulin also stimulates the synthesis of glucokinase and moderates the degree of gluconeogenesis. In the diabetic patient, there is an aberration in the functioning of insulin. Prior to the 1950s, control of diabetes was based entirely on insulin therapy. Unfortunately, some patients developed complications and thus need for some other therapy was realized. Presently control of NIDDM relies on compounds from two classes--sulphonylureas and biguanides. Although these drugs are widely accepted as being efficacious in treating some diabetics, they are ineffective in many others. Consequently, testing of many chemicals and plant extracts has continued. The object of the present paper is to bring up-to-date information on the hypoglycemic activity of plants, above all the plants occurring in our country, and those who se hypoglycemic activity has been scientifically documented in a more detailed way. Recent theories on the mechanism of action of these plants are also discussed.
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PMID:[Plants with hypoglycemic effects]. 811 60

Non-insulin-dependent diabetes mellitus is a serious metabolic disorder that affects an estimated 16 million Americans. Among African American women, diabetes has reached epidemic proportions, with 1 in 4 black women 55 years and older having diabetes. It is only within the last decade that diabetes research has begun to examine racial differences in the etiology, treatment, and long-term complications of diabetes. This review bring together the research that focuses on African American women within the context of diabetes research in the general population. Particular emphasis is placed on diabetes risk factors, complications of diabetes, and pharmacologic and nonpharmacologic treatment approaches. Diabetes prevention and public health issues related to diabetes and the African American women are discussed. The literature reviewed points to the importance of screening and early detection of diabetes among high-risk African American women, as well as the need for improved quality of care and patient educational services and programs in diabetes appropriate to the needs of African American women.
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PMID:Diabetes in African American women: the silent epidemic. 942 97

Type 2 diabetes is a complex metabolic disorder characterized by peripheral insulin resistance and impaired beta cell function. Insulin resistance is inherited as a non-mendelian trait. In genetically predisposed individuals, resistance of skeletal muscle and adipose tissue to insulin action precedes the onset of clinical diabetes, and is thought to contribute to hyperglycaemia by leading to impaired beta cell function and increased hepatic glucose production. It is not clear whether beta cell and liver defects are also genetically determined. To test the hypothesis that insulin resistance in muscle and fat is sufficient to cause type 2 diabetes in the absence of intrinsic beta cell and liver abnormality, we generated transgenic mice that were insulin-resistant in skeletal muscle and adipose tissue. These mice developed all the prodromal features of type 2 diabetes but, despite the compounded effect of peripheral insulin resistance and a mild impairment of beta cell function, failed to become diabetic. These findings indicate the need for a critical re-examination of the primary site(s) of insulin resistance in diabetes.
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PMID:Impaired glucose tolerance in mice with a targeted impairment of insulin action in muscle and adipose tissue. 980 35

Type 2 diabetes mellitus is a common metabolic disorder whose prevalence is increasing in the western world. The ravaging complications of the disease constitute a major cause of hospitalisation and cardiovascular morbidity, and despite intensive research the pathogenic mechanism remain unknown. The article summarises some recent advances in the field of islet beta-cell dysfunction caused by hyperlipidaemia in the diabetic state, which results in perturbed insulin secretory capacity and overt glucose intolerance. In contrast to hyperglycaemia, the detrimental effects of hyperlipidaemia have been a relatively neglected area of diabetes research. However, the direct inhibitory effects of long-term hyperlipidaemia on beta-cell function, 'lipotoxicity,' should form the basis of a more active approach to lipid screening and pharmacological treatment of hyperlipidaemia in diabetes patients. Intervention in the leptin pathway may prove beneficial in future treatment strategies.
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PMID:[Time for more active lipid-lowering treatment of patients with diabetes. Negative effect of hyperlipidemia on beta-cells is a neglected field]. 988 94

The hallmark of type 2 diabetes, the most common metabolic disorder, is a defect in insulin-stimulated glucose transport in peripheral tissues. Although a role for phosphoinositide-3-kinase (PI3K) activity in insulin-stimulated glucose transport and glucose transporter isoform 4 (Glut4) translocation has been suggested in vitro, its role in vivo and the molecular link between activation of PI3K and translocation has not yet been elucidated. To determine the role of PI3K in glucose homeostasis, we generated mice with a targeted disruption of the gene encoding the p85alpha regulatory subunit of PI3K (Pik3r1; refs 3-5). Pik3r1-/- mice showed increased insulin sensitivity and hypoglycaemia due to increased glucose transport in skeletal muscle and adipocytes. Insulin-stimulated PI3K activity associated with insulin receptor substrates (IRSs) was mediated via full-length p85 alpha in wild-type mice, but via the p50 alpha alternative splicing isoform of the same gene in Pik3r1-/- mice. This isoform switch was associated with an increase in insulin-induced generation of phosphatidylinositol(3,4,5)triphosphate (PtdIns(3,4,5)P3) in Pik3r1-/- adipocytes and facilitation of Glut4 translocation from the low-density microsome (LDM) fraction to the plasma membrane (PM). This mechanism seems to be responsible for the phenotype of Pik3r1-/- mice, namely increased glucose transport and hypoglycaemia. Our work provides the first direct evidence that PI3K and its regulatory subunit have a role in glucose homeostasis in vivo.
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PMID:Increased insulin sensitivity and hypoglycaemia in mice lacking the p85 alpha subunit of phosphoinositide 3-kinase. 998 80

The clinical features of polycystic ovary syndrome (PCOS) include hirsutism and irregular menses, which are the results of ovarian hyperandrogenism and chronic, unopposed estrogen secretion. The discovery that most women with PCOS are insulin-resistant and have compensatory hyperinsulinemia, with increased risk for type 2 diabetes mellitus, designates this condition as a reproductive-metabolic disorder. That the symptoms of PCOS may be mimicked by other endocrine disorders of the ovary and adrenal glands warrants careful evaluation to exclude these associated conditions.
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PMID:Diagnosis of polycystic ovary syndrome. 1035 25


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