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Query: UMLS:C0011854 (type 1 diabetes)
 20,749 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twelve healthy men with IDDM participated in a 12-week walking/jogging exercise program. Pre- and postexercise assessment of dietary intakes, body composition, biochemical measures, and exercise performance indicators were completed. Subjects exercised either 3 or 5 days per week for 1 hour at 60% to 80% of estimated maximal heart rate. Dietary intakes showed a voluntary reduction in fat intake as a percent of total energy from 40% +/- 7% (mean +/- SD) to 37% +/- 8% (P = .053). No change occurred over time in body composition measures except for a significant reduction in the waist-to-hip ratio from 0.87 +/- 0.04 to 0.86 +/- 0.04 (P = .007). Fasting serum glucose and lipid levels did not change over time. Exercise capacity improved, as shown by an increased time to exhaustion on a treadmill run from 7.9 +/- 3.7 minutes to 9.7 +/- 3.8 minutes (P less than .001); and a lower heart rate at a constant work load--from 183 +/- 18 beats per minute preexercise to 175 +/- 20 beats per minute postexercise (P = .022). The study showed that healthy male subjects with IDDM can benefit from regular exercise with a redistribution of body fat and improved exercise capacity.
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PMID:Benefits of exercise training for men with insulin-dependent diabetes mellitus. 201 25

Platelet function (as production of thromboxane B2 by platelets stimulated with collagen, and plasma beta-thromboglobulin) and thrombin activity (as plasma fibrinopeptide A) were investigated in eight young (mean age 27 +/- 3 SE years) male patients in which type 1 diabetes mellitus had been diagnosed 2 to 6 months previously. They were all in excellent stable metabolic control (mean HbA1c 5.6 +/- 0.4 SE %) and free from any complications. The haemostatic variables were assessed at rest and after cycloergometric exercise to exhaustion. When compared to age- and sex-matched healthy controls, patients showed higher beta-thromboglobulin, fibrinopeptide A and thromboxane B2 at rest. After exercise, plasma beta-TG increased only in the controls. Platelet and thrombin activation are present in the very early stages of type 1 diabetes mellitus, in the absence of any complications.
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PMID:Primary platelet activation in recent-onset type 1 diabetes mellitus. 214 55

In this study, in vitro B-cell models are described, which may be applicable for studying the reported B-cell desensitization produced by hyperglycemia in IDDM and NIDDM. Using a programmable perifusion/perfusion system, insulin secretion from perifused islets was measured at 10-30-min intervals for 24-50 h. After 3-4 h continuous glucose (11 mM), a new phase of insulin release occurs in which secretion declines to, and remains at, approximately 25% maximal release. Results were similar when using: perifused islets embedded in Cytodex 3, or Bio-Gel P-2, 100-200 mesh; batchincubated islets with hourly changes of medium; and the isolated pancreas perfused for 8 h. Three different media, Hana HB 104 (fortified, fully defined medium), RPMI-1640 + 10% FBS, and perfusion bufferalbumin, were used. Despite reduced secretion to continuous glucose, each system responded vigorously to an acute stimulation with glucose-forskolin. Decreased secretion was primarily caused by decreased secretagogue efficiency (reduced fractional secretion). Prolonged stimulation with glucose or glucose-IBMX produced a similar waning of secretion regardless of the amount of insulin released. It is concluded that the third phase of insulin secretion may represent a secret-agogue-induced, signal desensitization of the B-cell, rather than exhaustion of a B-cell compartment of stored insulin.
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PMID:The third phase of in vitro insulin secretion. Evidence for glucose insensitivity. 351 47

A literature survey and hypothesis is presented in which it is concluded that an intracellular ventromedial hypothalamic (VMH) glucopenia results in a bibrachial response consisting of adenohypophysial release of growth hormone and ACTH as well as sympathetic discharge, both of which act to elevate plasma glucose and remove the VMH glucopenia. This glucopenia may occur as a result of either a deficiency of circulating insulin or alterations in the kinetic properties of the VMH cellular insulin receptor. Two mechanisms for the development of insulin dependent diabetes mellitus (IDDM) are presented: (1) a defect in VMH glucose transport and/or metabolism such that a VMH glucopenia occurs with a subsequent bibrachial response. The result of this is glucose overproduction and a chronic excess glucose stimulus will eventually cause B-cell exhaustion (primary hypothalamic involvement). (2) reduction of the B-cell population by chemical, genetic and/or viral interactions with a consequential insulopenia results in a VMH glucopenia (secondary to a reduced glucose transport into the VMH cells) and causes a bibrachial response. This VMH response may temporarily restore plasma glucose balance but a chronically enhanced counter-regulatory response to maintain this balance will eventually stress the remaining B-cell population and cause further reductions in B-cell numbers (secondary hypothalmic involvement).
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PMID:A mechanism by which primary or secondary hypothalamic involvement results in the development of insulin-dependent diabetes mellitus (IDDM). 639 50

The relationships between psychosocial adjustment and subsequent glycaemic control were prospectively examined in forty-three adult patients during the first 2 yr after onset of type 1 diabetes mellitus. Decreasing depression was the single psychosocial parameter that changed over time. No correlations were found between the decrease in HbA1c levels and psychological variables at 8- and 16-month follow-ups. Global and specific coping features such as high control attitude, low coping anxiety and low emotional attribution correlated significantly with the decrease in HbA1c levels at the 2-yr follow-up, whereas stressful life events, depression, state-trait anxiety did not correlate. In a regression analysis coping explained 22% variance of the 2 yr decrease in HbA1c levels. We conclude that coping is a better predictor for metabolic control than emotional adaptation and life events. Metabolic control might deteriorate with prolonged stage of the disease being a first sign for psychophysiological coping exhaustion.
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PMID:Psychological moderator variables and metabolic control in recent onset type 1 diabetic patients--a two year longitudinal study. 802 64

Most of diabetics have no symptoms and chemical analyses may be sole way to diagnose the disease itself and its complications. Chemical analyses are also important to assess the propriety of glycemic control during every possible treatment of diabetes. Some markers for long-term glycemic control other than glucose concentration may be also used as a screening methods for glucose intolerance. HbA1c is established for long term as a marker for glycemic control but still large interlaboratory variation is present. Fructosamine is measured by a simpler procedure but many deoxidizing materials in serum especially superoxide may interfere with the reaction. Glycated albumin should be more reliable than fructosamine but a standard method of measurement has not been established yet. The decrease in serum 1,5-anhydro-D-glucitol(1,5-AG) is very sensitive to urinary glucose excretion and may be useful as a marker of glycemic control and diagnosis of diabetes. Discrimination of Type I(IDDM) from Type II(NIDDM) in Japanese diabetic patients is sometimes very difficult and evidences of autoimmunity by anti-glutamic acid decarboxylase(GAD) antibody and of exhaustion of insulin secretion by C-peptide measurement 6min after combined infusion of 1mg of glucagon and 20ml of 50% glucose are the few methods to diagnose. Early diagnosis of diabetic complication is another important point of clinico-chemical determinations. Usually, each diabetic complication progresses in parallel. Micro-measurement of urinary transferrin is one of the most sensitive methods likewise urinary microalbumin measurement. Future measurement of advanced glycation end product (AGE) may also tell us if patients are suffering from diabetic complications or if one is suffering from diabetes or not.
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PMID:[Recent progress in diagnoses of diabetes and its complications]. 856 34

This single-centre study investigated parameters that positively correlated with the success rate after islet allotransplantation in insulin-dependent diabetic (IDDM) patients. Twenty-one intrahepatic, fresh islet transplantations were performed in 20 IDDM patients (one patient had two transplants), after or simultaneous with kidney transplantation. The correlation between number and purity of transplanted islets and final outcome was investigated. One patient died of a cardiac arrest several hours after islet transplantation; this patient was not included in the follow-up analysis. Three patients (15%) experienced acute, irreversible, early failure of islet function, which was considered as a 'presumed rejection'. Nine patients (45%) achieved either complete insulin-independence (seven cases) or a reduction (> 50%) of exogenous insulin requirement (two cases), with sustained serum C-peptide secretion (0.89 +/- 0.04 nmol/l; duration: 21 +/- 7 months, range 2-58 months). Liver biopsy, performed 3 years after transplantation in one successful case, showed normal islets within the hepatic parenchyma. Eight cases (40%) did not show any metabolic effect of islet transplantation, with low serum C-peptide levels ('presumed function exhaustion'). Metabolic investigations performed in successful cases showed an early phase of insulin release after arginine, mild and reversible postprandial hyperglycaemia and normal HbA1c levels. Success of islet transplantation positively correlates with the number (p < 0.05) of the transplanted islets. Islet transplantation is a safe procedure, with 45% success rate, in terms of insulin-independence or relevant reductions of exogenous insulin requirement, although success can be transient.
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PMID:Islet transplantation in IDDM patients. 904 85

The annual pilgrimage to Makkah (Mecca), Hajj, is a very stressful endeavour and requires strenuous physical effort, especially for the diabetic, the elderly and persons with other chronic illnesses. To identify the complications and to assess the needs of the Omani diabetics during Hajj (DOH), a special diabetes clinic was established in the camping site of Omani pilgrims (Hajjees) in Mina, where all Omani Hajjees convene for three days. The socio-demographic characteristics, the diabetes profile and the knowledge about complications of diabetes of all DOH were ascertained; their random blood sugar (RBS) was tested. Of 10,800 Omani who performed the Hajj in 1996, the 169 Hajjees with diabetes mellitus (prevalence rate 16 per 1000) included four per cent insulin dependent (IDDM), seven per cent on dietary control, and 89% on oral hypoglycaemic agents. Almost all DOH (98%) were medically examined before their departure for Hajj. All Hajjees with IDDM and 96% on oral hypoglycaemic agents brought their medicines with them. During the Hajj period, 2.4% of DOH had RBS < 75 mg/dl, 14% 75-110 mg/dl, and 49% were hyperglycaemic (RBS > 200 mg/dL). About half of the DOH (48%) knew the clinical presentation of hyperglycaemia, a fourth (24%) about symptoms of hypoglycaemia. Only 9.5% were trained to test themselves for blood sugar. The median age of DOH was 54 years (inter-quartile range 50-62). Some 7.5% females and 4.9% of males were obese (body mass index > 30). Forty seven (28%) of the DOH had other coronary heart diseases, hypertension or both. DOH moved between Holy places (four journeys; 5-15 km long) on foot (40%), by car or bus (31%), or both (29%). All DOH except one were not wearing protective shoes, 70% did not have identification wrist bands that show their diabetic status and regimen for treatment. Four per cent lost their way during Hajj, four per cent suffered from heat exhaustion, three per cent had cut wounds, 1.2% had pneumonia, and two per cent went into coma. There is a need for a special health education programme and for special services for the diabetics during Hajj. Hajjees should learn about symptoms and signs of hypoglycaemia, were protective shoes and identifying wrist bands. Specialised services for the diabetics would alleviate a lot of the stress during Hajj among the diabetics.
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PMID:Profile of diabetic Omani pilgrims to Mecca. 974 36

In intense exercise (>80% VO(2max)), unlike at lesser intensities, glucose is the exclusive muscle fuel. It must be mobilized from muscle and liver glycogen in both the fed and fasted states. Therefore, regulation of glucose production (GP) and glucose utilization (GU) have to be different from exercise at <60% VO(2max), in which it is established that the portal glucagon-to-insulin ratio causes the less than or equal to twofold increase in GP. GU is subject to complex regulation by insulin, plasma glucose, alternate substrates, other humoral factors, and muscle factors. At lower intensities, plasma glucose is constant during postabsorptive exercise and declines during postprandial exercise (and often in persons with diabetes). During such exercise, insulin secretion is inhibited by beta-cell alpha-adrenergic receptor activation. In contrast, in intense exercise, GP rises seven- to eightfold and GU rises three- to fourfold; therefore, glycemia increases and plasma insulin decreases minimally, if at all. Indeed, even an increase in insulin during alpha-blockade or during a pancreatic clamp does not prevent this response, nor does pre-exercise hyperinsulinemia due to a prior meal or glucose infusion. At exhaustion, GU initially decreases more than GP, which leads to greater hyperglycemia, requiring a substantial rise in insulin for 40--60 min to restore pre-exercise levels. Absence of this response in type 1 diabetes leads to sustained hyperglycemia, and mimicking it by intravenous infusion restores the normal response. Compelling evidence supports the conclusion that the marked catecholamine responses to intense exercise are responsible for both the GP increment (that occurs even during glucose infusion and postprandially) and the restrained increase of GU. These responses are normal in persons with type 1 diabetes, who often report exercise-induced hyperglycemia, and in whom the clinical challenge is to reproduce the recovery period hyperinsulinemia. Intense exercise in type 2 diabetes requires additional study.
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PMID:Intense exercise has unique effects on both insulin release and its roles in glucoregulation: implications for diabetes. 1181 92

Type 1 diabetes is an autoimmune disease leading to a progressive exhaustion of the insulin secretion and a destruction of the B-cells. Attempts of preservation of insulin-producing B-cells can be performed at an early, most often silent, stage of the disease in well-selected at high risk subjects or during the period immediately following the clinical diagnosis based upon classical signs of hyperglycaemia. In the "Diabetes Prevention Trial-Type 1", the prophylactic subcutaneous administration of low-dose ultralente insulin was not able to prevent the development of type 1 diabetes nor to preserve residual insulin secretion in young relatives at very high-risk of diabetes, selected upon genetic, immunological and metabolic criteria. In contrast, a pilot randomized trial shows that a treatment with a nonactivating humanized monoclonal antibody against CD3 mitigates the deterioration in insulin production and improves metabolic control, with lower dose of exogenous insulin, during the first year of type 1 diabetes mellitus in 9 out of 12 treated patients. Besides a better understanding of the natural history of the disease, these clinical trials open new perspectives for prevention of type 1 diabetes mellitus, currently assessed by the Belgian Diabetes Registry.
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PMID:[Clinical study of the month. Attempt at preservation of B cells during the initial phase of type 1 diabetes: negative results with ultralente insulin, but promising results with an anti-CD3 monoclonal antibody]. 1218 38


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