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

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

The prevalence and clinical features of diagnosed mellitus secondary to chronic pancreatitis (CP) were assessed from northern (Hokkaido) to southern (Okinawa) Japan by means of a questionnaire to elucidate whether WHO-classified malnutrition-related diabetes mellitus (MRDM) exists in Japan. Of a total 17,500 diabetic patients, only two (0.011%)-one fibrocalculous pancreatic diabetes (FCPD) and one protein-deficient pancreatic diabetes (PDPD) - exhibited MRDM characteristics. A total of 649 CP were collected and classified into 268 cases with chronic alcoholic pancreatitis (CAP), 150 cases with chronic calcified pancreatitis (CCP) and 231 cases with other CP. The prevalence of diabetes mellitus was found to be 50.7% in CAP, 72.7% in CCP and 22.8% in other CP. Among all diabetics, 56.6% was noninsulin-dependent (NIDDM) and 26.4% insulin-dependent (IDDM). IDDM was most frequent in CP. Satisfactory and less than satisfactory glycemic control was obtained in approximately three quarters of all subjects. Only one quarter showed poor glycemic control. Insulin treatment was frequent in CAP (52.2%) and CCP (61.7%), but less in other CP (27.5%). The prevalence of diabetic retinopathy was observed in 33.1% of all subjects, nephropathy 21.0% and neuropathy 36.3%, respectively. The prevalence of complications, including macroangiopathy tended to be higher in CAP and CCP (40.3 and 56.9%) than in other CP (31.4%).
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PMID:Prevalence and clinical features of diabetes mellitus secondary to chronic pancreatitis in Japan; a study by questionnaire. 224 5

For the simultaneous evaluation of insulin secretion and insulin sensitivity, a glucose regulation model has been developed. In order to estimate the parameters of the model, an intravenous glucose infusion test (GIT, 100 mg/kg.min x 2 min and 10 mg/kg.min x 118 min) was carried out on 15 healthy subjects (N), 12 subjects with impaired glucose tolerance (IGT), 20 non-insulin-dependent diabetics (NIDDM) and 13 patients with chronic pancreatitis (CP). The coefficient (microU/mg) for insulin secretion depending on blood glucose concentration in IGT, NIDDM and CP were lower (35.9 +/- 2.7, 24.5 +/- 3.3, 43.1 +/- 3.1) than in N (77.5 +/- 7.9). The coefficients (microU.min/mg) for insulin secretion depending on rate of change in blood glucose concentration in IGT and NIDDM were significantly lower (6.5 +/- 2.1, 3.8 +/- 1.2) than in N (52.8 +/- 8.8). The insulin sensitivity index (ISI; 10(-2) mg/(microU/ml).kg.min) in NIDDM was lower (4.98 +/- 0.75) than in N (11.37 +/- 1.08). Administration of exogenous insulin did not significantly affect the value of ISI in N and NIDDM. ISI showed a tendency to increase (15.09 +/- 1.92) in CP. It was demonstrated that the proposed model which estimates both insulin secretory ability and insulin sensitivity simultaneously is quite useful for analyzing the mechanism of impaired glucose tolerance.
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PMID:Simultaneous evaluation of insulin secretion and action using a model. 264 38

The nomenclature of human diabetes mellitus (DM) has been revised, and this classification has been accepted throughout the medical world and literature. The major categories of diabetes are: insulin-dependent DM, type I or IDDM; noninsulin-dependent DM, type II or NIDDM; secondary DM or type S; impaired glucose tolerance, IGT; gestational diabetes; and previous abnormality of glucose tolerance, PrevAGT. A review of the literature has shown that over half of the documented diabetic dogs, with a single medical diagnosis, appear to be type I, IDDM, with a substantial proportion being type S, and the remainder being type II, NIDDM. Obesity is frequently associated with IGT and NIDDM. Diabetic cats most commonly have pancreatic islet destruction associated with pancreatic amyloidosis; they are insulin deficient, IDDM. The commonest causes of secondary diabetes in dogs are pancreatic damage, hyperadrenocorticism and hypersomatotropism secondary to persistent progesterone influence. Progestogen therapy is the most frequently reported cause of secondary diabetes in cats. Diabetes in horses is type S, usually secondary to a functional pituitary tumor but occasionally following chronic pancreatitis. The blood glucose ranges for normal, IGT and diabetic animals, and the normal serum insulin values of various species is tabulated.
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PMID:Definition of diabetes mellitus. 351 69

The literature with respect to GIP is flooded with conflicting data especially with respect to its role in type 2 diabetes mellitus, obesity, type 1 diabetes mellitus and chronic pancreatitis. This review describes possible reasons for the discrepancies which include species variation of GIP, heterogeneity of molecules with different immunoreactivity and bioactivity, deterioration of immunoreactivity of standard and sample on prolonged storage and the effect of the preceding intake of type and quantity of food. The problems can be resolved by raising antibodies to synthetic human GIP and its fragments, the chemical characterization of and the raising of antibodies to immunoreactive GIP 8000, the correct storage of samples and the standard preparation of subjects prior to experimental procedures.
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PMID:Conflicting gastric inhibitory polypeptide data: possible causes. 847 32

NIDDM is a heterogeneous disease and subgroups of NIDDM include MODY (Maturity Onset Diabetes of the Young), Malnutrition-related diabetes (MRDM) and Fibrocalculus pancreatic diabetes (FCPD). Endocrine cell population is relatively unchanged in NIDDM: B-cells are reduced by up to 30% and A-cells increased by 10%. Islet amyloid is found in 96% of subjects occupying up to 80% of the islet associated with a reduction in B-cells. Amyloid formation is unlikely to cause diabetes but progressive accumulation increases the severity of the disease. Islet amyloid is formed from the islet amyloid polypeptide (IAPP), a normal constituent of B-cells, co-secreted with insulin. The causal factors for IAPP fibrillogenesis are unknown but abnormal synthesis or overproduction could be involved: stimulation of B-cell secretion in NIDDM by obesity, hyperglycaemia or suphonylurea therapy may promote amyloidosis and further aggravate islet pathology. A mutation of the glucokinase gene in MODY leads to diminished B-cell secretion but not amyloid formation. Diabetes and mutations of mitochondrial DNA is associated with poorly developed islet structure. Exocrine pancreatic size is reduced and there is evidence of sub-clinical chronic pancreatitis in NIDDM. In MRDM and FCPD, chronic pancreatitis and exocrine necrosis is associated with reduced insulin secretion. Unlike cystic fibrosis where islet amyloid is present in diabetic individuals, amyloid is absent from subjects with FCPD. Pathological changes in the exocrine and endocrine pancreas in NIDDM results from and contributes to the pathophysiology of insulin secretion in NIDDM.
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PMID:Pancreatic pathology in non-insulin dependent diabetes (NIDDM). 852 18

Most cases of diabetes mellitus result from decreased insulin secretion (type I, insulin-dependent) or altered insulin action (type II, insulin-independent). Another category, namely, "other" diabetes mellitus-associated conditions, is usually mentioned to distinguish this type of diabetes from the other two categories; this category includes drugs, genetic and endocrine syndromes, and pancreatic disorders. The most common pancreatic disease that causes diabetes mellitus is chronic pancreatitis that results from alcohol abuse. The clinical observation of patients at our institution with long histories of heavy alcohol intake and diabetes mellitus prompted us to review the impact of alcohol on carbohydrate metabolism. In many of these patients, it was notable that they were not obese and they had no immediate family members with diabetes mellitus, raising the possibility that alcohol-associated diabetes mellitus may be a distinct subset of non-insulin-dependent diabetes mellitus that is distinct from type II diabetes mellitus.
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PMID:Alcohol-associated diabetes mellitus. A review of the impact of alcohol consumption on carbohydrate metabolism. 876 12

To compare the clinical usefulness of commercial radioimmunoassay (RIA) kits based on recombinant and pig brain GAD, we measured glutamic acid decarboxylase autoantibody (GADAb) titers in 125 non-obese (body mass index < 24) Japanese diabetics without insulin therapy using two commercial RIA kits based on recombinant human (rh) GAD65 (GADAb Cosmic) and purified pig brain native GAD (RIP Anti-GAD Hoechst). The frequencies of GADAb positivity using these two RIA kits (normal ranges; < 1.3 and < 4.0 U/ml, respectively) were about 4.8 (6/125) and 3.2% (4/125), respectively. The six patients found to be positive with RIA using GADAb Cosmic demonstrated significantly higher prevalence of NIDDM in their parents (P = 0.04), lower beta-cell function estimated by intravenous glucagon loading tests (P = 0.03) and higher prevalence of progression to insulin therapy (P = 0.0001). Five of these six patients slowly progressed to insulin-requiring status within 34 +/- 11 months of follow-up evaluation, and one of these five patients progressed to a completely insulin-dependent status within 30 months from the onset of diabetes. Of these six patients, two demonstrated chronic pancreatitis, three had chronic thyroiditis, and five showed HLA DR4. Interestingly, two of the six patients demonstrated very low GADAb titers (2.3 and 2.9 U/ml), while RIP Anti-GAD Hoechst showed no positivity with the same sera. Based on the binding study after pre-incubation of unlabeled GADs, these low titrated GADAb were elucidated to be true specific reactions to rh GAD65 alone. Moreover, one of the two patients with chronic thyroiditis and HLA DR4 slowly progressed to insulin-requiring status over a period of 45 months. These findings suggest that the measurement of GADAb using a commercial assay kit with rh GAD65 may be more useful to detect non-insulin-dependent type I diabetics among non-obese patients than using a commercial kit with purified pig brain native GAD, especially among those with low GADAb titers.
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PMID:Antibodies to glutamic acid decarboxylase (GAD) in non-obese Japanese diabetics without insulin therapy: a comparison of two commercial RIA kits based on recombinant and pig brain GAD. 976 69

Diabetes mellitus secondary to chronic pancreatitis is characterized by a progressive destruction of the pancreas, including loss of the islet cells, leading to a form of diabetes that can mimic both type 1 and type 2 diabetes. Glucagon-like peptide 1(7-36)amide (GLP-1), an intestinally derived insulinotropic hormone, represents a potential therapeutic agent for type 2 diabetes, because exogenous GLP-1 has been shown to increase the insulin and reduce the glucagon concentrations in these patients, and thus induce lower blood glucose, but without causing hypoglycemia. Ten patients with diabetes mellitus secondary to chronic pancreatitis and five normal subjects were studied. Nine patients were treated with insulin and one patient with sulfonylurea. In the fasting state, saline or GLP-1 in doses of 0.4 or 1.2 pmol/min/kg body weight were infused intravenously for 4 hours. Blood glucose was reduced in all patients with both doses of GLP-1; plasma C-peptide increased (p<0.02), and plasma glucagon decreased (p<0.02) compared with basal levels, also in three patients with normoglycemia and high levels of presumably exogenous insulin. Similar results were obtained in the normal subjects. In conclusion, GLP-1 treatment may be considered in patients with diabetes mellitus secondary to chronic pancreatitis, provided that a certain amount of alpha- and beta-cell secretory capacity is still present.
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PMID:Effect of glucagon-like peptide 1(7-36)amide in insulin-treated patients with diabetes mellitus secondary to chronic pancreatitis. 1063 Mar 80

Reduced exocrine pancreatic function has been observed in a high percentage of patients with type 1 diabetes in the past. There are only few data for type 2 diabetes available and they are contradictory. In this study we investigated exocrine pancreatic function in 105 controls and 114 patients with type 1 or type 2 diabetes mellitus by means of an indirect test (faecal elastase-1 concentration). This test has good sensitivity and specificity for moderate and severe pancreatic insufficiency as compared to the gold standard. Reduced faecal elastase-1 concentrations were found in 56.7% of type 1 patients, 35% of type 2 patients and 18.1% of the controls. Elastase-1 concentrations did not correlate with alcohol consumption, diabetes duration or diabetes therapy. The data found for type 1 patients correspond to those reported in earlier studies. The results for type 2 diabetics show that exocrine pancreatic function is also impaired in a high percentage in this group of patients. Pathogenetic concepts to explain these findings as consequences of diabetes complications or insulin deficiency are still under debate. Observations from autopsies and the data of the controls in this study suggest that chronic pancreatitis might be a common problem. In consequence, diabetes secondary to exocrine disease could be much more frequent than believed so far.
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PMID:Pancreatic exocrine function in patients with type 1 and type 2 diabetes mellitus. 1127 9


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