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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Glucose tolerance and insulin responses have been examined over extended periods in severely obese, but otherwise healthy, subjects. Three significant points emerge from this study. First, it was shown that obese, supposedly ketosis resistant, subjects may deteriorate in a brief time span from a state of normal glucose disposal and adequate or increased insulin responses to insulin-deficient diabetes, culminating in ketoacidosis. Unusually high blood glucose levels complicating the ketoacidosis in two patients suggest hyperosmolarity obesity and added risk factor in severely obese diabetics. It appears that, after long-standing obesity and after years of hyperinsulinemia, a large weight gain due to prolonged overeating may impose an excessive challenge to islet cells of marginal competence. Such an event by itself or a superimposed stress or both may then cause acute insulin deficiency and/or insulin resistance leading to diabetic ketoacidosis. Hyperosmolarity may be exacerbated in the obese with cessation of food intake due to large losses of salt and water. Second, many symptoms and manifestations of hyperphagic obesity are similar to the early functional abnormalities of decompensated diabetes. The advent of the critical phase of uncontrolled diabetes, therefore, fails to alarm the obese patient and may escape timely recognition by the physician. Third, technical and mechanical difficulties due to severe obesity are apt to cause critical delays in therapy. These factors, when added to coexisting hyperosmolarity and ketoacidosis, probably account for the high mortality in these patients.
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PMID:Evolution of diabetic ketoacidosis in gross obesity. 80 48

Hypertension is associated with hyperinsulinemia in the presence or absence of obesity or glucose intolerance. Physiological concentrations of insulin decrease the catecholamine-induced production of prostaglandin I2 (PGI2; prostacyclin) and PGE2, two potent vasodilators, in adipose tissue, one of the largest organs in the body. This finding suggests that hyperinsulinemia increases peripheral vascular resistance and blood pressure by inhibiting the stimulatory effect of adrenergic agonists (and perhaps other agonists) on the production of PGI2 and PGE2 in adipose tissue (and perhaps other tissues). This concept is supported by evidence that PGI2 and PGE2 modulate vascular reactivity in states of health and disease. For example, during insulin deficiency, i.e., in diabetic ketoacidosis, PGI2 and PGE2 production by adipose tissue are increased, and peripheral vascular resistance and blood pressure are decreased. This hypothesis is also supported by evidence that blood flow through rat and human adipose tissue is decreased in obesity and that insulin decreases the blood flow through adipose tissue in nonobese rats. Thus, insulin may regulate PGI2 and PGE2 production by adipose tissue (and possibly other tissues) through a wide range of concentrations with important physiological and clinical consequences.
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PMID:Insulin, prostaglandins, and the pathogenesis of hypertension. 193 84

448 Sudanese diabetics were included in this study. 30% of patients were in the age group 40-50 years and only 6.3% had childhood diabetes. The predominant sex was female (64.5%). Obesity was found in 39% of patients, a positive family history in 66.5% and a history of diabetic ketoacidosis in 25.2%. 100 patients (below the age of 40) had a plain X-ray abdomen done but none had evidence of pancreatic calcification. Percentages of diabetic complications in this study were as follows: neuropathy 28.1%, retinopathy 18.5%, cataract 14.7%, hypertension 12.9%, nephropathy 11.6%, peripheral vascular disease 6.2%, coronary heart disease 4.2% and pulmonary tuberculosis 2.7%. The majority of our patients were uncontrolled, only 16.7% had normoglycaemia (FBG less than 140 mg%).
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PMID:Pattern of diabetes mellitus in the Sudan. 263 51

[3-14C]acetoacetate (AcAc) and beta-[3-14C]hydroxybutyrate (beta-OHB) administration, measurements of labeled AcAc and beta-OHB in blood, and kinetic modeling have been used to investigate ketone body (KB) metabolism in five normal, five obese, and eight insulin-withdrawn diabetic subjects. Diabetic subjects were divided in mildly ketotic (MKD) and highly ketotic (HKD) patients according to beta-OHB blood level. A four-compartmental model successfully described the tracer kinetic data in obese and normal subjects, whereas in diabetic patients a five-compartmental model was necessary. Obese subjects showed a significantly lower (P less than 0.05) KB de novo synthesis (R30 = 159 +/- 54 (SD) mumol X min-1 X m-2) in comparison with normal subjects (282 +/- 93), but the clearance rates of AcAc (PCR1) and beta-OHB (PCR2) were similar in the two groups. R30 was 596 +/- 534 in MKD and 1,278 +/- 445 (P less than 0.01) in HKD. PCR1 was not significantly different both in MKD and HKD in comparison with normal subjects. In contrast PCR2 was markedly reduced in HKD (0 +/- 0 ml X min-1 X m-2) in comparison with MKD (1,031 +/- 615) and normal subjects (782 +/- 278). The percentage distribution of KB among various tissues inside the organism of diabetic subjects is abnormal. Both AcAc and beta-OHB recycling and mean residence time are not normal in HKD. A significant correlation was found between C-peptide and KB production in diabetes. These results suggest that a selective defect of beta-OHB peripheral utilization is important in determining and maintaining severe diabetic ketoacidosis.
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PMID:Acetoacetate and 3-hydroxybutyrate kinetics in obese and insulin-dependent diabetic humans. 392 34

With the awareness of health problems related to obesity, weight reducing diets have become very popular. However, if these meal supplements are not taken as recommended, they can cause considerable harm in high risk individuals. We report a case of a young obese man who developed diabetic ketoacidosis (DKA) followed by rhabdomyolysis and acute renal failure (ARF) after excessive intake of a high carbohydrate containing weight-reducing meal. DKA associated with excessive intake of weight reducing diets has not been reported previously. In people with obesity and insulin resistance improper use of these supplements can cause severe metabolic complications.
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PMID:Diabetic ketoacidosis and rhabdomyolysis following excessive intake of a weight reducing diet. 971 84

PURPOSE: To contrast incidence rates and time trends of typical type 1 diabetes with non-autoimmune insulin-resistant type 2 diabetes in minority children (Early 2).METHODS: A population based registry of all insulin treated African-American and Hispanic children residing in Chicago, aged 0-17 years at onset, diagnosed between 1985-1994 provided data. Medical records were reviewed and abstracted (N = 739), and a subset of patients were interviewed (n = 195). Based on these data sources, cases were assigned to the early type 2 category if one or more of the following variables were present: notation of "atypical" or "possible type 2" diabetes in the medical record; obesity (defined as BMI >/= 27 (kg/m(2))) or acanthosis nigricans noted at diagnosis; a report by the patient of going off insulin six months after initial diagnosis without developing diabetic ketoacidosis; or reporting the use of oral hypoglycemic agents with or without insulin. The Chi-square test for homogeneity was used to determine differences between proportions of groups. Time trend analysis of incidence was done using regression models with the Poisson distribution.RESULTS: The 10-year average annual incidence rate was 10.3 per 100,000 population for typical type 1 diabetes (n = 565) and 3.2 per 100,000 for those with characteristics of early 2 diabetes (n = 174). Over the ten year interval the incidence rate remained static for typical type 1 diabetes. In the early 2 group there was a 9.0% average annual percent increase over the ten year interval (p < 0.01).CONCLUSIONS: The trends in incidence rates vary between typical type and early 2 diabetes. We hypothesize that this is associated with the increasing rate of obesity and a lack of physical activity in young people.
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PMID:Are trends in diabetes incidence changing for minority children? 1101 69

Insulin-dependent diabetes mellitus (IDDM) can lead to ventilatory depression and decreased sensitivity to hypercapnia. We examined relationships between ventilation, plasma insulin, leptin, ketones, and blood glucose levels in two mouse models of IDDM: (1) streptozotocin-induced diabetes in C57BL/6J mice on a regular diet or with induced obesity from a high fat diet; and (2) spontaneous diabetes mellitus in NOD-Ltj mice. In both mouse models, IDDM resulted in depression of the hypercapnic ventilatory response (HCVR). This ventilatory depression was not associated with decreases in plasma insulin or leptin levels. There was, however, a strong association between the duration of hyperglycemia, the decline in HCVR, and increased glycosylation of the diaphragm. Hyperventilation was observed in only six of 14 C57BL/6J obese wild-type mice, despite a significant degree of diabetic ketoacidosis (DKA) in all 14 animals. In mice with DKA, there was a significant correlation between the increase in baseline minute ventilation (V E) and hyperleptinemia (r = 0.77, p < 0.01). In leptin-deficient C57BL/6J-Lep(ob) mice, low levels of both V E and ketones were observed. These results suggest that: (1) depression of the HCVR in IDDM is associated with hyperglycemia and glycosylation of the diaphragm; and (2) the hyperventilation of DKA is leptin dependent.
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PMID:The impact of insulin-dependent diabetes on ventilatory control in the mouse. 1125 15

A 31-year-old woman was admitted to our hospital because of diabetic ketoacidosis (DKA). Ultrasound sonography revealed the existence of the left adrenal tumor and endocrinological examinations established a diagnosis of pheochromocytoma. She had been healthy and there was no evidence for gestational diabetes in her personal history. Characteristic features were not found in her tumor size and the catecholamine levels as compared with typical cases of pheochromocytoma. An overwhelming secretion of catecholamine might suppress insulin secretion, as evidenced by the improvement after the resection of the tumor. However, a significant insulin resistance continued after tumor resection. Obesity and the heterozygosity of beta3-adrenergic receptor gene (Try64Arg) might play a role in insulin resistance, which resulted in DKA at least in part. Literature survey revealed four cases of DKA in the patients with pheochromocytoma including ours, three of which were Japanese. Pancreatic capacity to secrete insulin has been reported to be less than Caucasians, which might be another reason for DKA. Thus, we speculate that both suppressed insulin secretion and insulin resistance deteriorated by obesity or other factor(s) such as abnormality in beta3 adrenergic receptor probably depress beta-cell function resulting in abnormal metabolic imbalance such as DKA.
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PMID:Diabetic ketoacidosis in a case of pheochromocytoma. 1164 Sep 97

In 9 years (1990-1998), 40 Arab patients between the ages of 0 and 18 years had newly diagnosed diabetes mellitus (DM) at the Al-Ain hospital, United Arab Emirates (UAE). In this cohort, 35 patients had Type 1 DM while the remaining five patients had features of early onset Type 2 DM. For Type 1 DM patients, the mean age at diagnosis of was 9.2+/-4.1 years. At presentation, their mean plasma glucose was 27.6+/-11/mmol with 28 (80%) patients having diabetic ketoacidosis (DKA), both being much higher than generally reported in the West. The mean insulin requirement increased from 0.84+/-0.27 U/kg per 24 h (0-9-year group) to 1.02+/-0.33 U/kg per 24 h (10-18-year group), P=0.055. The home glucose monitoring and the glycaemic control of these Type 1 DM patients were sub-optimal with 28% of patients having recurrence of DKA. Among the Type 2 DM patients, four (80%) were obese with a positive family history of Type 2 DM. All of them initially responded to diet and oral hypoglycaemic drugs. Public education about DM in childhood and prevention of adolescent obesity remain major public health challenges in the UAE.
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PMID:Childhood and adolescent diabetes mellitus in Arabs residing in the United Arab Emirates. 1175 76

Type 2 diabetes mellitus and impaired glucose tolerance are associated with antipsychotic treatment. Risk factors for type 2 diabetes and impaired glucose tolerance include abdominal adiposity, age, ethnic status, and certain neuropsychiatric conditions. While impaired glucose metabolism was first described in psychotic patients prior to the introduction of antipsychotic medications, treatment with antipsychotic medications is associated with impaired glucose metabolism, exacerbation of existing type 1 and 2 diabetes, new-onset type 2 diabetes mellitus, and diabetic ketoacidosis, a severe and potentially fatal metabolic complication. The strength of the association between antipsychotics and diabetes varies across individual medications, with the largest number of reports for chlorpromazine, clozapine, and olanzapine. Recent controlled studies suggest that antipsychotics can impair glucose regulation by decreasing insulin action, although effects on insulin secretion are not ruled out. Antipsychotic medications induce weight gain, and the potential for weight gain varies across individual agents with larger effects observed again for agents like chlorpromazine, clozapine, and olanzapine. Increased abdominal adiposity may explain some treatment-related changes in glucose metabolism. However, case reports and recent controlled studies suggest that clozapine and olanzapine treatment may also be associated with adverse effects on glucose metabolism independent of adiposity. Dyslipidemia is a feature of type 2 diabetes, and antipsychotics such as clozapine and olanzapine have also been associated with hypertriglyceridemia, with agents such as haloperidol, risperidone, and ziprasidone associated with reductions in plasma triglycerides. Diabetes mellitus is associated with increased morbidity and mortality due to both acute (e.g., diabetic ketoacidosis) and long-term (e.g., cardiovascular disease) complications. A progressive relationship between plasma glucose levels and cardiovascular risk (e.g., myocardial infarction, stroke) begins at glucose levels that are well below diabetic or "impaired" thresholds. Increased adiposity and dyslipidemia are additional, independent risk factors for cardiovascular morbidity and mortality. Patients with schizophrenia suffer increased mortality due to cardiovascular disease, with presumed contributions from a number of modifiable risk factors (e.g., smoking, sedentary lifestyle, poor diet, obesity, hyperglycemia, and dyslipidemia). Patients taking antipsychotic medications should undergo regular monitoring of weight and plasma glucose and lipid levels, so that clinicians can individualize treatment decisions and reduce iatrogenic contributions to morbidity and mortality.
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PMID:Hyperglycemia and antipsychotic medications. 1180 85


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