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

Effective fuel metabolism is dependent on balances among exogenous and endogenous fuel availability, the glucagon/insulin ratio, and tissue insulin sensitivity. Diabetes mellitus results when imbalances occur. The resultant metabolic derangement is accompanied by abnormalities in carbohydrate, protein, and fat metabolism. The two most common forms of diabetes are insulin dependent (IDDM) and noninsulin dependent (NIDDM). IDDM is an autoimmune disease, characterized by insulinopenia and ketosis. NIDDM is related to impaired insulin secretion, defective tissue sensitivity, and abnormalities in glucose transporter proteins. This article describes normal fuel metabolism and traces the abnormal metabolic processes that lead to both IDDM and NIDDM.
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PMID:Normal fuel metabolism and alterations in diabetes mellitus. 184 Sep 66

Diabetes mellitus is composed of a heterogeneous group of disorders characterized by high blood glucose levels. Four major types of diabetes have been defined by the National Diabetes Data Group. Insulin-dependent diabetes (IDDM), also called type I diabetes, is characterized by abrupt clinical onset, insulinopenia, proneness to ketosis even in the basal state, and dependence on exogenous insulin to sustain life. Non-insulin-dependent diabetes (NIDDM), also called type II diabetes, may remain relatively asymptomatic for years. Insulin levels may be normal, lower than normal, or elevated as a consequence of insulin resistance. Ketosis is not part of the general clinical picture except in times of metabolic stress, although the classic complications of diabetes can be expected to develop in long-duration diabetics. Gestational diabetes (GDM) refers to the recognition of abnormal glucose intolerance in pregnancy, although unrecognized abnormal tolerance may indeed have predated the pregnancy. Rates of macrosomia are higher than in non-GDM pregnancies, but fetal mortality and congenital anomalies appear to be no greater than in the general population. Other types of diabetes include a number of diverse conditions in which glucose intolerance is a feature and in which it may be etiologically related. Impaired glucose tolerance (IGT) is a class that encompasses persons whose glucose tolerance is intermediate between normal and diabetic. These individuals do not manifest the microvascular complications of diabetes, but they appear to have higher rates of macrovascular disease associated with the known cardiovascular risk factors. Two statistical risk categories have also been defined that replace the older terms prediabetes, potential diabetes, and latent diabetes. Diabetes can be diagnosed by the presence of classical signs and symptoms of diabetes and unequivocally elevated blood glucose levels; by a fasting plasma glucose greater than or equal to 140 mg/dl; or by an abnormal oral glucose tolerance test, with a venous plasma glucose value greater than or equal to 200 mg/dl at 2 hours after 75 grams oral glucose, being a hallmark criterion for diabetes. For the latter two criteria, the abnormality should be reconfirmed at a later occasion before a definitive diagnosis of diabetes is made. The oral glucose tolerance test has been standardized at a 75-gram glucose (or carbohydrate equivalent) load, given in the morning after an overnight fast. Glucose should be determined for two hours after administration of the challenge.
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PMID:Classification and diagnostic criteria for diabetes mellitus and other categories of glucose intolerance. 329 Sep 16

Serum C-peptide levels were measured during a glucagon stimulation test in ten normal nonobese controls and 54 diabetic patients with recent onset of diabetes under 30 years of age. Diabetic patients were comprised of 13 CTPD, 23 IDDM, and 18 NIDDM. As similar to IDDM patients, serum C-peptide concentrations did not rise significantly (P greater than 0.05) in response to glucagon administration in CTPD-patients. Mean baseline and peak serum C-peptide concentrations in CTPD-patients were significantly lower (P less than 0.001) than the values in normal controls and NIDDM patients, but were significantly higher (P less than 0.05) than those in IDDM patients. We conclude that CTPD patients have partial C-peptide reserve, which may protect against ketosis and contribute to ketosis resistance in CTPD. Our results also suggest that CTPD patients require insulin treatment. Neither baseline nor peak C-peptide levels after glucagon could discriminate CTPD from IDDM and CTPD from NIDDM.
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PMID:C-peptide secretion in calcific tropical pancreatic diabetes. 352 43

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

Patients with type II diabetes mellitus (type II DM patients) are characteristically obese, hyperinsulinemic, and non-ketosis prone. Recently, we have encountered several obese type II DM patients with either diabetic ketoacidosis or significant ketonuria after insulin withdrawal. There was no evidence of infection, stress, or starvation to explain their ketonuria. Therefore, we assessed serum connecting peptide (C-peptide) response to oral glucose in 14 obese, insulin-treated type II DM patients: 6 with and 8 without episodes of spontaneous ketonuria. The group presenting with ketonuria had low to absent basal and stimulated serum C-peptide responses. The nonketonuric group had higher basal C-peptide (P less than 0.01) concentrations that increased significantly (P less than 0.001) after oral glucose compared with those of the ketonuric group. Clinical characteristics and biochemical control were similar in both groups. Our findings confirm that obese type II diabetes mellitus is a heterogeneous disease with variable fasting and stimulated C-peptide responses. Spontaneous ketonuria could be a feature in the clinical presentation of the patients especially in the presence of both low fasting and stimulated C-peptide levels. The significance of these findings is unclear but suggests individualization in the management of type II DM patients and cautious withdrawal of insulin therapy in such patients. Furthermore, serum C-peptide levels alone cannot be recommended to classify patients into either type I or type II diabetes mellitus.
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PMID:Significance of spontaneous ketonuria and serum C-peptide levels in obese type II diabetic patients. 638 58

Non-insulin-dependent diabetes mellitus (NIDDM) with onset below 35 years of age was studies in 43 Indian and 9 Black patients. NIDDM was diagnosed in 10.0% and 1.6% of diabetes in the respective racial groups. The mean age of the patients was 35.4 years and the mean duration of diabetes 7.5 years. Nearly 50% of patients were significantly obese, and more than 50% had a positive family history of diabetes. In all patients the diabetes was symptomatic at presentation, although frequently insidious in onset. In all cases the symptoms could be controlled without insulin therapy. Despite persistence significant hyperglycaemia in several patients, ketosis did not occur at any stage. Complications were detected in 40% of the Indian and 22% of the Black patients, but were unrelated to the duration of diabetes or severity of hyperglycaemia. Basal insulin levels and postglucose insulinaemic responses were lower in the Black than the Indian diabetes.
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PMID:Non-insulin-dependent diabetes mellitus with early onset in Blacks and Indians. 702 Jan 2

A 63-year-old woman with NIDDM poorly controlled by insulin therapy was admitted to our hospital because of fever and severe lumbago. Laboratory data revealed diabetic ketosis and a hypercoagulable state with infection. Bone and gallium scintigrams revealed an abnormal accumulation of the isotopes at L4-L5, where magnetic resonance imaging showed inflammatory changes. The patient was then diagnosed as having pyogenic vertebral osteomyelitis. Antibiotic chemotherapy and the administration of gebexate mesilate improved the inflammation and hypercoagulable state. When diabetic patients suffer from severe lumbago with sustained fever, and show segmental knock pain along the spine, pyogenic vertebral osteomyelitis should be considered. Bone and gallium scintigrams, and MRI are of clinical value for the early diagnosis of the disease.
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PMID:A case of non-insulin-dependent diabetes mellitus with vertebral osteomyelitits: usefulness of imaging diagnosis. 859 15

Autoantibodies to 65 kD glutamic acid decarboxylase (GADAA) and ICA512 (ICA512AA) were measured by radioimmunoassays using as antigens in vitro transcribed and translated [35S]-methionine-labeled human GAD65 and ICA512 (IA-2). The prevalence of GADAA and ICA512AA in sera from 87 patients with IDDM was 39 and 23%, respectively. The frequency and titer of ICA512AA declined sharply within 5 years after the onset of IDDM. Among patients tested within 4 years after diagnosis, the prevalence of ICA512AA was significantly higher in acute onset IDDM than in slowly progressive IDDM (37 versus 6%, P < 0.025) irrespective of age, while there was no difference in GADAA frequency between acute onset and slowly progressive subtypes (51 versus 63%). A total of two patients out of 121 patients with NIDDM were positive for GADAA, and two other NIDDM patients, who were suffering from sarcoidosis, were positive for ICA512AA. Neither of the antibodies were positive in sera from four atypical NIDDM patients, aged < 20 years, who showed ketosis at onset and required insulin followed by excellent metabolic control with diet restriction alone. These observations suggest that ICA512AA are associated with rapid progression of beta cell damage in IDDM. ICA512 radioassay, in combination with GAD assay may provide a useful diagnostic marker for IDDM especially in youth.
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PMID:Combined measurements of GAD65 and ICA512 antibodies in acute onset and slowly progressive IDDM. 917 63

Differentiating NIDDM-Y from IDDM in youth is a diagnostic challenge. Serum insulin levels at diagnosis may help differentiate between NIDDM-Y and IDDM if the level is elevated, but the serum insulin level is low or undetectable in 45% of patients with NIDDM-Y. Islet-specific antibodies may be present in serum at diagnosis, and ketosis or ketoacidosis may occur. For our patients, clinical features are most helpful in differentiating NIDDM-Y from IDDM and include ethnic background, age and gender at diagnosis (approximately 80% of First Nation patients from northern Manitoba are adolescent females), presence of obesity and acanthosis nigricans, lack of symptoms or weight loss, and strong family history of NIDDM.
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PMID:Diagnostic criteria for non-insulin dependent diabetes in youth (NIDDM-Y). 949 13

Forty-three cases of diabetic ketosis were analysed to determine the mode of presentation, treatment modalities and outcome. Among these cases 62.8% were non-insulin dependent diabetes mellitus (NIDDM) patients and 37.2% belonged to the insulin dependent diabetes mellitus (IDDM) group. Six patients had blood glucose levels of more than 250 mg/dl but less than 300 mg/dl who were grouped separately for analysis under the term "euglycaemic diabetic ketoacidosis (EGDK)". Infection was the commonest precipitating factor in diabetic ketosis in all groups. Abdominal pain and vomiting occurred with NIDDM and EGDK cases. Drowsiness was common and coma was rare. Acute myocardial infarction (MI) and pulmonary oedema occurred with NIDDM cases. Shock, acidosis, acquired respiratory distress syndrome (ARDS) and mucor mycosis were seen with IDDM cases. Mortality was 7 out of 43(16.3%). Saline requirement was lower in NIDDM and EGDK cases. Intensive insulin therapy with hourly intravenous doses were needed for IDDM cases while majority of NIDDM cases could be managed with 6 hourly doses of insulin given subcutaneously or intramuscularly.
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PMID:Changing profile of diabetic ketosis. 956 97


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