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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To test the hypothesis that 'vital exhaustion' (VE), a state characterized by unusual fatigue, increased irritability, and feelings of demoralization, precedes the onset of myocardial infarction (MI) in females, 79 females hospitalized with a first MI (mean age: 59.3; SD = 9.3) and 90 females hospitalized in the departments of general and orthopaedic surgery (mean age: 57.4; SD = 9.1), were compared on the retrospective form of the Maastricht Questionnaire (MQ). Defining 'exhaustion' as a score above the median of the MQ, 63% of the cases and 39% of the controls were exhausted before hospitalization (chi 2 = 10.02; p < 0.00). The relative risk associated with exhaustion, after controlling for age, smoking, coffee consumption, diabetes, hypertension, non-anginal pain, and menopausal status, was estimated as 2.75 (95% CI:I.28-5.81; p < 0.01), thus corroborating the hypothesis. Exploratory analyses of the origins of exhaustion in these females showed that of all biographical characteristics, holding a job and simultaneously taking care of the household was most strongly associated with elevated exhaustion scores.
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PMID:Vital exhaustion as risk indicator for myocardial infarction in women. 790 33

Hyperglycemia with accompanying hyperinsulinemia occurs after brief, greater than 85% maximum oxygen consumption exercise to exhaustion in normal subjects and persists up to 60 min of recovery. To determine the importance of endogenous insulin secretion during and after intense exercise, responses to exercise of lean fit male post-absorptive insulin-dependent diabetes mellitus (IDDM) subjects, aged 18-34 yr, were compared with those of control subjects (C; n = 6). Three iv insulin protocols were employed: hyperglycemic (HG; n = 7) and euglycemic (EG1; n = 6) with constant insulin infusion, and euglycemic with doubled insulin infusion during recovery (EG2; n = 6). Overnight iv insulin was adjusted to achieve prolonged euglycemia (5.4 +/- 0.3 mmol/L) or hyperglycemia (8.6 +/- 0.3 mmol/L) before exercise. This allowed for comparisons between HG and EG1 (constant infusion) and between C and EG2 (to approximate physiological hyperinsulinemia by doubling the infusion rates at exhaustion for 56 +/- 7 min during recovery). Subjects exercised to 89-98% of their individual maximum oxygen consumption for 12.8 +/- 0.3 min. Glycemia increased to maximum values at 6 min of recovery (9.8 +/- 0.5 in HG, 6.9 +/- 0.4 in EG1, 7.3 +/- 0.3 in EG2, and 6.9 +/- 0.4 mmol/L in C). Whereas in EG2 and C, glucose returned to resting values in 50-80 min, it remained elevated at 120 min recovery in HG and EG1. During exercise, [3-3H]-glucose-determined glucose production increased markedly and exceeded disappearance in all groups, but less so in the HG subjects than in the other groups. An early recovery decline in glucose production did not differ among groups, but MCR (rate of glucose disappearance/glycemia) were markedly lower in HG and EG1, in whom plasma free insulin remained unchanged from 15 min of recovery onward (MCR, 1.6-1.9 vs. 2.3-2.8 mL/kg.min in C). Doubling the insulin infusion rate in EG2 restored the MCR response to that of C subjects. In summary, constant insulin infusion is insufficient to prevent prolonged postexercise hyperglycemia in IDDM subjects, even when provided at a rate sufficient to maintain normal resting glycemia and glucose turnover. The finding that increasing the rate of insulin infusion restored plasma glucose to normal in IDDM subjects suggests that the postexercise increase in insulin levels observed in normal subjects is essential to return plasma glucose to resting levels. Therefore, special strategies, differing from those for less strenuous exercise, are required for the management of insulin therapy in IDDM during and after intense exercise.
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PMID:Hyperinsulinemia prevents prolonged hyperglycemia after intense exercise in insulin-dependent diabetic subjects. 796 73

To elucidate the pathogenesis of diabetes in spontaneously diabetic Chinese hamsters (CHAD strain), a longitudinal study from just after weaning to overt diabetic state was performed. Fasting and non-fasting plasma glucose, non-fasting plasma insulin and pancreatic hormone contents (insulin, glucagon and amylin) were measured, and light microscopic examination of pancreatic islets by immunohistochemical technique and pancreas perfusion study were performed. No insulitis was found in the islets of the CHAD strain. In animals aged 1 month, there was no significant difference in the percentage of B-cell area to islet area between the CHAD strain and the control. At this stage, hyperinsulinemia was observed despite normal plasma glucose levels both in fasting and non-fasting states. In the animals of the CHAD strain aged 2-4 months, insulin secretion from the pancreas, pancreatic insulin content and non-fasting plasma insulin level decreased in proportion to the decrease of B-cell mass. In animals aged about ten months, severe hyperglycemia and hypoinsulinemia were observed. We demonstrated the existence of amylin-like immunoreactivity in the B-cells of Chinese hamsters. However, no amyloid deposit was observed in the islets of the CHAD strain. After the onset of diabetes, amylin secretion from the pancreas and pancreatic amylin content in the CHAD strain were significantly lower than those in the control. We demonstrated the natural history of B-cell dysfunction in the CHAD strain. It could mean the process of B-cell exhaustion. The profile of the CHAD strain is similar to some types of human NIDDM. Therefore, the CHAD strain is a useful diabetic model in the study of NIDDM.
Diabetes Res Clin Pract 1994 Jul
PMID:Natural history of B-cell dysfunction in spontaneously diabetic Chinese hamsters. 798 44

Instability of the system of detoxication of peroxidative products and system of generation of free-radical oxidation of membrane lipids in placenta, funic blood, in amniotic water of mothers with diabetes mellitus and in newborns blood has been found. It is shown, that the exhaustion of antioxidative status of fetoplacental complex connected with the depression of antioxidative activity in blood of the newborns reflects the frustration of adaptation reaction of the newborn's organism, that may increase the risk of perinatal diseases or mortality.
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PMID:[Role of antioxidant enzymes of the fetoplacental complex in neonatal adaptation to maternal diabetes mellitus]. 799 48

It is found that antioxidative activity (AOA) and activity of glutathione-transferase in postmitochondrial placenta fraction of pregnant women with diabetes mellitus is lowered. Depression of AOA in placenta associated with a decrease of UDA and ceruloplasmin amount in blood of the newborns shows the exhaustion of the antioxidative protection system. A decrease of enzyme activity at the sorbitol way of glucose exchange (sorbitol-dehydrogenase and aldose reductase) in placenta reflects accumulation of sorbitol in tissue, which intensifies the damage of membrane structures in placenta.
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PMID:[Status of the antioxidant system and sorbitol pathway of glucose metabolism in diabetes mellitus]. 823 22

Insulin action is highly likely to be primarily genetically determined (given a permissive or facilitative environment, for example sufficient calorie availability), as shown by variations in ethnic distribution, evidence for familial transmission and genotypic responses to experimentally induced metabolic stresses. Further, it is likely that the genetic predisposition to insulin resistance is closely linked to (or perhaps synonymous with) the predisposition to develop overt NIDDM. Alternatively, in the development of diabetes, the genetic basis for insulin resistance may be necessary, but not sufficient, requiring a second major gene for beta-cell vulnerability (e.g. exhaustion, deterioration of function, amyloid deposition). The future examination of the genetics of insulin action depends in large measure on the method of assessment of insulin action that is selected and its consistent application to individuals, families and populations. The phenomenological approaches currently being used to describe and define insulin resistance could be identifying many different disorders, all leading to an apparent decrease or impairment of insulin action compared with that in 'normals'. Selection of any method for determining the presence of insulin resistance, together with selection of the threshold for 'present versus absent' is, at best, difficult. It is further complicated by the frequent association of insulin resistance with a wide range of disturbances, including hypertension, dyslipidaemia and glucose intolerance--the insulin resistance 'syndrome'. A number of possible loci and candidate genes controlling insulin action have been studied, and most have been ruled out as the probable underlying cause of the majority of cases of defective insulin action. Among those genes that are unlikely to be determinants of insulin resistance (except in a few rare cases of mutations) are those for insulin, the insulin receptor, glucose transporters and the genes for many specific enzymes. While these are unlikely to be responsible for insulin resistance, such potential genetic defects cannot be fully excluded using present methods. Direct gene sequencing of polymerase-chain-reaction amplified DNA may be the ultimate approach to identifying the critical defects underlying insulin resistance. Other candidate genes regulating insulin action are likely soon to come forth, such as those controlling the generation and function of the intracellular mediators of insulin action.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Genetics of insulin action. 830 12

Diabetes is more common in Aborigines than in other Australian populations, even in groups that have lived in contact with Europids for 150 years. Prevalence data on hyperinsulinaemia and obesity from urbanized south eastern Australian Aborigines are presented with Europid comparisons. Aborigines had higher mean insulin levels than Europids. In females, mean fasting insulin was 15.5 mU/l in Aborigines, compared with 9.5 mU/l in Europids (P < 0.001). The means for males were 15.1 mU/l (Aborigines) and 8.3 (Europids) (P < 0.005). Obesity was more prevalent in Aborigines. In Aboriginal females aged 25-64 years, 41/108 (38%) had BMI > 30.0, compared with 37/208 (18%) Europids (P < 0.001). In males, the difference in the prevalence of obesity in Aborigines (17/69, 25%) and Europids (34/195, 17%) was not statistically significant. Waist-hip ratio was significantly greater among Aboriginal females (mean 0.87 in persons aged 25-64 years) than among Europids (mean 0.81, P < 0.001). In males, the mean ratio in Aborigines and Europids was the same (0.94). Abdominal obesity was most prevalent among Aboriginal females. For females aged 20-49 years, 83/110 (75%) Aborigines had a waist-hip ratio > 0.80, compared with 71/165 (43%) Europids (P < 0.001). Being overweight or obese is perceived with least accuracy by Aboriginal males of the four ethnicity/gender groups. Comparisons with national data suggest a gradient in the prevalence of obesity, lowest in urban groups, more in the country, and higher still among Aborigines, which is in reciprocal order to socio-economic status. In multivariate analyses, the association of BMI with insulin was highly significant. Hyperinsulinaemia in an Aboriginal group after many years of contact with Europids may result from environmental as well as genetic influences. Relative hyperinsulinaemia is not found among those Aborigines who have developed glucose intolerance, which could be explained by earlier pancreatic exhaustion in this group.
Diabetes Res Clin Pract 1993 May
PMID:Hyperinsulinaemia and obesity in aborigines of south-eastern Australia, with comparisons from rural and urban Europid populations. 837 69

Intense exercise is associated with a marked stimulation of glucose production (Ra), a somewhat smaller increment in its utilization (Rd) (and therefore hyperglycemia), large increases in plasma catecholamines, and moderate hyperglucagonemia. The hyperglycemia increases in recovery and is accompanied by hyperinsulinemia. Because these adaptations are unique to intense exercise, we tested the physiological significance of the hyperinsulinemia by exercising six fit, postabsorptive young male subjects with insulin-dependent diabetes mellitus (IDDM) after overnight glycemic normalization by iv insulin, keeping its infusion rate constant during and for 2 h after 100% maximum VO2 cycle ergometer exercise to exhaustion (12 min) (no postexercise hyperinsulinemia). Their responses were compared with those of matched control subjects studied on two separate occasions, once without intervention (physiological hyperinsulinemia, n = 6) and again with a 0.05 U/kg iv bolus at exhaustion (postexercise supraphysiological hyperinsulinemia, n = 5). In all three study protocols, Ra increased by 7-fold, and Rd by 4-fold at exhaustion, and Ra declined in early recovery at the same rates. Therefore, the early recovery hyperinsulinemia is not required to return Ra to preexercise levels, and excessive hyperinsulinemia does not accelerate this decline. We infer that the catecholamine increments and decrements are the prime regulators of Ra (correlations of Ra vs. norepinephrine or epinephrine, P < 0.001 in the three studies), with a smaller contribution from the concurrent hyperglucagonemia. Rd, in contrast, was significantly affected by insulin. In the IDDM subjects, Rd remained at the same rate as Ra through most of recovery, resulting in sustained hyperglycemia and decreased glucose MCR, vs. the control subjects. This hyperglycemia compensated for the abnormal MCR, such that Rd was comparable to that in the control subjects. With the insulin bolus, the Rd elevation was sustained longer compared to the study without bolus, resulting in mild hypoglycemia successfully counterregulated by an increase in Ra. Thus, the principal regulators of the marked exercise increase and rapid recovery decrease in Ra are probably the catecholamines. The postexercise hyperinsulinemia is required for the MCR response and to return plasma glucose concentrations to preexercise levels. Different therapeutic strategies are required in persons with IDDM undergoing strenuous vs. moderate exercise, because of their inability to generate the postexercise hyperinsulinemia.
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PMID:The roles of insulin and catecholamines in the glucoregulatory response during intense exercise and early recovery in insulin-dependent diabetic and control subjects. 844 12

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

The widespread distribution of enzymes classed as semicarbazide-sensitive amine oxidases (SSAO enzymes) throughout a very wide range of eukaryotic as well as prokaryotic organisms encourages the aspirations of those who wish to demonstrate physiological, pathological or pharmacological importance. Such enzymes are found in several tissues of mammals, both freely soluble, as in blood plasma, and membrane-bound, for example, in smooth muscle and adipose tissue. While they are capable of deaminating many amines with the production of an aldehyde and hydrogen peroxide, doubt still surrounds the identity of the most important endogenous substrates for these enzymes. At present, methylamine and aminoacetone appear to head the list of candidates. The possibility that SSAO enzymes can convert amine substrates to highly toxic metabolites is illustrated by the production of acrolein from the xenobiotic amine, allylamine and formaldehyde and methylglyoxal from methylamine and aminoacetone, respectively. Activities of SSAO enzymes may be influenced by physiological changes, such as pregnancy or pathologically by disease states, including diabetes, tumours and burns. Increased deamination of aminoacetone by tissue and plasma SSAO enzymes as a result of its increased production from L-threonine in conditions such as exhaustion, starvation and diabetes mellitus may be harmful. Such dangers could be mitigated either physiologically by a compensatory reduction in SSAO activity or pharmacologically by treatment with inhibitors of SSAO.
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PMID:Some aspects of the pathophysiology of semicarbazide-sensitive amine oxidase enzymes. 858 67


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