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

Gastric emptying is a major determinant of glycemia, gastrointestinal hormone release, and appetite. We determined the effects of different intraduodenal glucose loads on glycemia, insulinemia, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and cholecystokinin (CCK), antropyloroduodenal motility, and energy intake in healthy subjects. Blood glucose, plasma hormone, and antropyloroduodenal motor responses to 120-min intraduodenal infusions of glucose at 1) 1 ("G1"), 2) 2 ("G2"), and 3) 4 ("G4") kcal/min or of 4) saline ("control") were measured in 10 healthy males in double-blind, randomized fashion. Immediately after each infusion, energy intake at a buffet meal was quantified. Blood glucose rose in response to all glucose infusions (P < 0.05 vs. control), with the effect of G4 and G2 being greater than that of G1 (P < 0.05) but with no difference between G2 and G4. The rises in insulin, GLP-1, GIP, and CCK were related to the glucose load (r > 0.82, P < 0.05). All glucose infusions suppressed antral (P < 0.05), but only G4 decreased duodenal, pressure waves (P < 0.01), resulted in a sustained stimulation of basal pyloric pressure (P < 0.01), and decreased energy intake (P < 0.05). In conclusion, variations in duodenal glucose loads have differential effects on blood glucose, plasma insulin, GLP-1, GIP and CCK, antropyloroduodenal motility, and energy intake in healthy subjects. These observations have implications for strategies to minimize postprandial glycemic excursions in type 2 diabetes.
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PMID:Load-dependent effects of duodenal glucose on glycemia, gastrointestinal hormones, antropyloroduodenal motility, and energy intake in healthy men. 1760 58

Social isolation is associated with increased risks of mortality and morbidity. In this study, we show that chronic individual housing accelerated body weight gain and adiposity in KK mice but not C57BL6J mice, and fully developed diabetes in KKA(y) mice. Individually housed KK and KKA(y) mice increased body weight gain over the initial 2 wk without increased daily average food consumption compared with group-housed animals. The individually housed KK and KKA(y) mice then gradually increased food consumption for the next 1 wk. The chronic social isolation-induced obesity (SIO) was associated with hyperleptinemia and lower plasma corticosterone and active ghrelin levels but not hyperinsulinemia. Elevated plasma leptin in the SIO suppressed expression of 5-HT2C receptor in white adipose tissue. The SIO was also associated with decreased expression of beta3-adrenergic receptors in white adipose tissue and hypothalamic leptin receptor, which might be secondary to the enhanced adiposity. Interestingly, social isolation acutely reduced food consumption and body weight gain compared with group-housed obese db/db mice with leptin receptor deficiency. Social isolation-induced hyperglycemia in KKA(y) mice was associated with increased expression of hepatic gluconeogenetic genes independent of insulin. These findings suggest that social isolation promotes obesity due to primary decreased energy expenditure and secondary increased food consumption, which are independent of the disturbed leptin signaling, in KK mice, and develops into insulin-independent diabetes associated with increased expression of hepatic gluconeogenetic genes in KKA(y) mice. Thus, social isolation can be included in the environmental factors that contribute to the development of obesity and type 2 diabetes.
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PMID:Social isolation affects the development of obesity and type 2 diabetes in mice. 1764 Sep 95

The patient, a 78-year-old female with a 10-year history of type 2 diabetes mellitus, was admitted to our department for evaluation of leg edema and general fatigue. Biochemical investigations revealed hypokalemia and elevated serum cortisol and plasma ACTH levels, with a loss of diurnal rhythm and failure of suppression at high doses (8 mg) of dexamethasone. No pituitary tumor or parasellar tumor was detected by contrast-enhanced computed tomography (CT) or magnetic resonance image scan of the pituitary. High resolution CT of the lung and bronchoscopic examination revealed no abnormalities. Abdominal and pelvic CT indicated bilateral, slightly diffuse, adrenal gland hyperplasia only. These findings led to a diagnosis of ACTH-dependent hypercortisolism from an undefined source. Ten days after admission the patient had a fever and was diagnosed with disseminated intravascular coagulation. Despite intensive treatment about 1 month after admission the patient died from progressive multiple organ failure. At autopsy, a histological examination of the periphery of the right middle lobe of the lung revealed the presence of tumorlets. Immunohistochemical staining of the tumorlets revealed scattered cells containing ACTH and many cells containing chromogranin A that were positive for Grimelius staining. In addition, multiple microabscesses were present throughout most tissues of the body. The ectopic hormonal production observed in the present case suggests that pulmonary tumorlets should thus be considered in the differential diagnosis of Cushing's syndrome, and medical treatment to inhibit steroidogenesis should be started immediately to reduce the risk of complications from hypercortisolism.
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PMID:Autopsy of a patient with Cushing's Syndrome who was revealed to have pulmonary tumorlets producing ectopic ACTH. 1800 Mar 46

A 71-year-old woman with type 2 diabetes mellitus complained of generalized fatigue. A 36-mm tumor in the pancreatic tail was detected with ultrasonography. The tumor was found to have marked hypervascularity with contrast-enhanced computed tomography (CT) and magnetic resonance. Combined (18)F-fluorodeoxyglucose positron emission tomography and CT ((18)F-FDG PET/CT) showed (18)F-FDG by the tumor with a maximal standardized uptake value of 2.98 at 50 min and 3.29 at 100 min following injection of (18)F-FDG. (18)F-FDG PET/CT suggested no extrapancreatic spread of the tumor. The patient had no pancreatic hormone-associated symptoms. Distal pancreatectomy was performed, and a well-differentiated endocrine tumor was diagnosed. The resected specimen showed neither infiltration of adjacent structures nor metastasis to regional lymph nodes. The present case suggests that (18)F-FDG PET/CT is a reliable modality for staging endocrine pancreatic tumors.
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PMID:Nonfunctioning endocrine pancreatic tumor examined with 18F-FDG PET/CT. 1831 38

Limited opportunity for movement and load-bearing exercise for conventionally caged laying hens leads to bone loss and increased susceptibility to osteoporosis, bone fractures, and cage layer fatigue, all of which compromise hen welfare and have negative consequences for production. The objective of this study was to compare bone mineral density (BMD) and strength measures of White Leghorns housed in conventional battery cages (CONV), cages modified to incorporate a nest box and perch (MOD), and commercially available, furnished colony cages with (CWDB) or without (CWODB) a raised dust bath. Hens reared on floor litter were randomly allocated to 1 of 4 cage systems at 19 wk of age. Hen-day production and egg quality were measured between 20 and 64 wk. At 65 wk, hens were killed, and right femur, tibia, and humerus were excised. Bone mineral density was assessed using quantitative computed tomography, and breaking strength was measured with an Instron Materials Tester. In the femur and tibia, CONV hens exhibited lower total BMD, bone mass, cortical bone area, cortical bone mass, and bone-breaking strength than CWDB, CWODB, and MOD hens. Density and cross-sectional area of bone in the trabecular space was highest in CONV. In the humerus, total and cortical BMD and mass and breaking strength values were higher for colony-housed birds than hens in CONV and MOD. The MOD birds did not exhibit increased humeral BMD or strength measures over CONV hens. These findings provide evidence that hens housed in modified and colony cages, furnished systems that promote load-bearing movement, are better able to preserve cortical structural bone than conventionally caged hens and simultaneously have stronger bones. Furthermore, inclusion of raised amenities that encourage wing loading is necessary to reduce humeral cortical bone loss. The overall absence of correlation between egg production or quality and bone quality measures also suggests that improved bone quality in CWDB, CWODB, and MOD furnished cages is not the result of lowered egg production or quality.
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PMID:Bone mineral density and breaking strength of White Leghorns housed in conventional, modified, and commercially available colony battery cages. 1842 Sep 72

Non-alcoholic fatty liver disease (NAFLD) covers a wide spectrum of liver pathology--from steatosis alone, through the necroinflammatory disorder of non-alcoholic steatohepatitis (NASH) to cirrhosis and liver cancer. NAFLD/NASH is mostly related with visceral adiposity, obesity, type 2 diabetes melitus (DM t.2) and metabolic syndrome. Pathogenetic concepts of NAFLD include overnutrition and underactivity, insulin resistance (IR) and genetic factor. The prevalence of NAFLD has been estimated to be 17-33% in some countries, NASH may be present in about 1/3 of such cases, while 20-25% of NASH cases could progress to cirrhosis. NAFLD is now recognized as one of the most frequent reason of liver tests elevation without clinical symptoms. Insulin resistance is considering as having a central role in NAFLD pathogenesis. In hepatocytes, IR is related to hyperglycaemia and hyperinsulinaemia, formation of advanced glycation end-products, increased free fatty acids and their metabolites, oxidative stress and altered profiles of adipocytokines. Early stages of fatty liver are clinically silent and include elevation of ALT and GGTP, hyperechogenic liver in USG and/or hepatomegaly. Among clinical symptoms, abdominal discomfort is relatively common as well as chronic fatigue. NAFLD/NASH is not a benign disease, progressive liver biopsy have shown histological progression of fibrosis in 32%, the estimated rate of cirrhosis development is 20% and a liver--related death is 12% over 10 years. No treatment has scientifically proved to ameliorate NAFLD or to avoid its progression. The various therapeutic alternatives are aimed at interfering with the risk factors involved in the pathogenesis of the disorder in order to prevent the progression to end-stage liver disease. The most important therapeutic measure is increasing insulin sensitivity by an attempt to change a lifestyle mostly by dieting and physical activity in order to loose weight. The most used agent is metformin, the others are under controlled trials or their effectiveness is low. NASH is not a common indication for liver transplantation because of the older age distribution of patients and high prevalence of comorbidity, related to metabolic syndrome. Recurence of NASH in the grafted liver is also a relatively frequent complication.
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PMID:[Non-alcoholic fatty liver disease--new view]. 1870 46

Hypogonadism is a common condition, especially among older men, but often goes undiagnosed and untreated. It can be associated with a number of signs and symptoms that affect health and quality of life, including feelings of low energy and fatigue; decreased sex drive and performance; decreased muscle mass and strength; decreased bone mineral density; and increased body fat, particularly abdominal fat, a putative risk factor for metabolic syndrome and type 2 diabetes mellitus. The evidence supporting testosterone replacement therapy (TRT) in improving these and related conditions is strong and consistent for body composition and sexual function; moderately consistent for bone mineral density; inconsistent for insulin sensitivity, glycemic control, and lipid profiles; and weak and inconsistent for mood and cognitive function. The concern of some physicians about the potential for TRT to stimulate prostate cancer is not supported by decades of data accumulated to date, though studies of longer duration (eg, 10 years or more) would be even more convincing. Other research needs are discussed. As the front line of health care delivery, primary care physicians need to be vigilant in diagnosing and treating symptomatic hypogonadism. Based on current guidelines, we recommend assessing testosterone levels when an adult man exhibits signs of hypogonadism, and as part of normal medical screening in men starting at age 40 to 50 years, to establish a baseline. A physician should discuss the possibility of TRT with symptomatic patients who have a serum total testosterone level < 300 ng/dL. If TRT is initiated, a patient's response and adverse events should be assessed every 3 to 6 months, and therapy adjusted accordingly.
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PMID:Testosterone replacement therapy in hypogonadal men: assessing benefits, risks, and best practices. 1882 32

Over half of all Australians are classified as overweight or obese and this is increasing by 1% of the population per year. Obesity is linked with a range of health ailments including type 2 diabetes, heart diseases and some cancers. At a population level it is well accepted that obesity is a result of the increasing use of modern technology, resulting in decreased energy expenditure, in combination with easily available high energy density foods, the "obesogenic environment". In the modern environment, there are two major areas of management to assist the overweight and obese. Both include a change in lifestyle. Future strategies in weight management should include reduction in energy density and increase in daily physical activity.
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PMID:Dealing with obesity: an Australian perspective. 1892 39

Our laboratory has investigated 2 hypotheses regarding the effects of fructose consumption: 1) the endocrine effects of fructose consumption favor a positive energy balance, and 2) fructose consumption promotes the development of an atherogenic lipid profile. In previous short- and long-term studies, we showed that consumption of fructose-sweetened beverages with 3 meals results in lower 24-h plasma concentrations of glucose, insulin, and leptin in humans than does consumption of glucose-sweetened beverages. We have also tested whether prolonged consumption of high-fructose diets leads to increased caloric intake or decreased energy expenditure, thereby contributing to weight gain and obesity. Results from a study conducted in rhesus monkeys produced equivocal results. Carefully controlled and adequately powered long-term studies are needed to address these hypotheses. In both short- and long-term studies, we showed that consumption of fructose-sweetened beverages substantially increases postprandial triacylglycerol concentrations compared with glucose-sweetened beverages. In the long-term studies, apolipoprotein B concentrations were also increased in subjects consuming fructose, but not in those consuming glucose. Data from a short-term study comparing consumption of beverages sweetened with fructose, glucose, high-fructose corn syrup, and sucrose suggest that high-fructose corn syrup and sucrose increase postprandial triacylglycerol to an extent comparable with that induced by 100% fructose alone. Increased consumption of fructose-sweetened beverages along with increased prevalence of obesity, metabolic syndrome, and type 2 diabetes underscore the importance of investigating the metabolic consequences of fructose consumption in carefully controlled experiments.
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PMID:Endocrine and metabolic effects of consuming beverages sweetened with fructose, glucose, sucrose, or high-fructose corn syrup. 1906 38

We report a rare case of Bartter's syndrome in a 35-year-old woman with type 2 diabetes mellitus. The patient presented with leg weakness, fatigue, polyuria and polydipsia. Hypokalemia, metabolic alkalosis, and high renin and aldosterone concentrations were present, but the patient was normotensive. Gitelman's syndrome was excluded because of the presence of hypercalciuria, secondary hyperparathyroidism and bilateral nephrocalcinosis. The patients condition improved upon administration of a prostaglandin synthetase inhibitor (acemetacin), oral potassium chloride and potassium-sparing diuretics. Five months later, the patient discontinued acemetacin because of epigastric discomfort; at the same time, severe hypokalemia and hyperglycemia developed. Glucagon stimulation and water deprivation tests were performed. Type 2 diabetes mellitus with nephrogenic diabetes insipidus was diagnosed. To avoid further gastrointestinal complications, the patient was treated with celecoxib, a selective cyclooxygenase 2 inhibitor. This case serves as a reminder that Bartter's syndrome is associated with various metabolic derangements including nephrogenic diabetes insipidus, nephrocalcinosis and diabetes mellitus. When treating Bartter's syndrome, it is also prudent to remember that the long-term use of nonsteroidal anti-inflammatory drugs and potassium-sparing diuretics may result in serious adverse reactions.
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PMID:Bartter's syndrome with type 2 diabetes mellitus. 1925 37


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