Development Of Diabetes In Patients Research Articles

Histologic Scores for Fat and Fibrosis Associate With Development of Type 2 Diabetes in Patients With Nonalcoholic Fatty Liver Disease.

Nonalcoholic fatty liver disease (NAFLD) is a strong risk factor for development of type 2 diabetes, but little is known about how long-term NAFLD or its histologic features affect risk. We aimed to investigate the cumulative incidence of type 2 diabetes in patients with NAFLD and to identify histologic factors that affect risk of diabetes. We performed a retrospective study of 396 patients in Sweden diagnosed with NAFLD by biopsy analysis from 1971 through 2009 who did not have type 2 diabetes at baseline. Data on development of type 2 diabetes were collected from patient charts and national registers. Patients were categorized into groups with fibrosis stages 0-2 (n= 357) or stages 3-4(n=39). Hazard ratios of histologic parameters for type 2 diabetes development were calculated separately in a multivariate Cox regression model adjusted for sex, age, body mass index, and serum levels of triglycerides greater than 150 mg/dL. During a mean follow-up period of 18.4 years (range, 0-41 years), 132 individuals (33%) developed type 2 diabetes. A significantly higher proportion of patients with fibrosis stages 3-4(51.2%) developed type 2 diabetes than patients with fibrosis stages 0-2 (31.3%) (P=.02). For patients with fibrosis stages 0-2, fat score associated independently with development of type 2 diabetes (adjusted hazard ratio, 1.34; 95% confidence interval, 1.03-1.74; P= .03). No histologic factors associated with development of diabetes in patients with fibrosis stages 3-4. Presence of nonalcoholic steatohepatitis was not associated with development of type 2 diabetes. In a retrospective study we found a higher proportion of patients with fibrosis stages 3-4 to develop type 2 diabetes than patients with fibrosis stages 0-2. In patients with fibrosis stages 0-2, fat score associates with risk of type 2 diabetes.

Intelligent system for diabetes prediction in patients with chronic pancreatitis

This paper presents the results of the JSM-method for automated support of scientific research (ASSR JSM-method) implemented in a computer intelligent system (IS-JSM), which predicts the development of diabetes in patients with chronic pancreatitis. For the first time the ASSR JSM-method is applied to a sequence of expanding databases of facts, which was used for the detection of empirical regularities (ERs), viz., preserved causes of the studied effect (development of diabetes in patients with chronic pancreatitis). To recognize ERs in the IS-JSM, we used an algebraic lattice of JSM-reasoning strategies (inductive inference rules). These results have an informative clinical interpretation and prove the usefulness of data mining using the IS-JSM, which can be used as a tool for evidence-based medicine.

Hepatitis C virus infection and diabetes

Hepatitis C virus (HCV) infection is the leading cause of chronic liver disease resulting in end-stage cirrhosis and liver cancer, and it remains the primary cause for liver transplantation in the western countries. Chronic HCV infection is believed to be a multi-faceted systemic disease which not only influences the hepatic environment causing inflammation, steatosis and fibrosis but also alters the metabolism of glucose and lipids, leading to metabolic sequelae such as insulin resistance, diabetes and dyslipidaemia. HCV has been identified as an independent risk factor for the development of diabetes in predisposed individuals (with family history and visceral obesity) and it is more prevalent with certain HCV genotypes. Moreover, it can also induce direct destruction of pancreatic β cells and trigger auto-immune reactions by molecular mimicry in the pancreas, leading to auto-immune diabetes. Its immunological effects can also lead to the development of diabetes in patients who had undergone liver transplantation for HCV infection which is further made worse by intense immunosuppression used in such settings. This article provides an overview of the intriguing relationship between HCV infection and diabetes, the two major public health challenges which lead to widespread health and financial burden worldwide. Copyright © 2016 John Wiley & Sons.

Increasing Timely Postpartum Oral Glucose Tolerance Test Completion in Women with Gestational Diabetes: A Quality-Improvement Initiative.

Gestational diabetes (GDM) is defined as hyperglycemia that is first recognized during pregnancy. It affects 5% of pregnancies, and higher rates occur in certain ethnic minorities (1). GDM increases the risk for the development of type 2 diabetes and other metabolic complications later in life. Of women with GDM, 4% will be diagnosed with type 2 diabetes, and 20% of womenwith GDMwill have developed type 2 diabetes within 10 years postpartum (2). Within the first 6 months after delivery, upwards of 25% of women will have persistent abnormalities in their postpartum glucose levels in the form of impaired glucose tolerance (IGT), which is detectable only by a formal 2-hour 75 g oral glucose tolerance test (OGTT) (3). Identification of IGT prior to a subsequent pregnancy is important because these women experience dysglycemia with the onset of pregnancy and require ongoing monitoring and treatment. The Canadian Diabetes Association guidelines recommend a 75 g OGTT 6 weeks to 6 months postpartum; however, the rates of compliance with this guideline are less than 20% (4). Diabetes and its complications are a major financial burden on the healthcare system and are associated with major morbidity for patients. Screening programs in this population have been shown to be cost saving and to improve quality of life (5). There is high-level evidence that intensive lifestyle interventions can prevent the development of diabetes in patients with impaired glucose tolerance (6). The diabetes-prevention program showed

Diabetes in Pediatric Patients with Kearns-Sayre Syndrome: Clinical Presentation of 2 Cases and a Review of Pathophysiology

Kearns-Sayre syndrome (KSS), resulting from a mitochondrial DNA deletion, is a rare cause of diabetes in children. We report 2 pediatric cases of KSS associated with diabetes that presented with hyperosmolar hyperglycemia with minimal ketosis. Both patients were treated initially with isotonic fluid resuscitation followed by intravenous insulin infusion. The first case was a boy of Blackfoot Aboriginal ancestry who presented with failure to thrive, developmental delay and Fanconi syndrome and was diagnosed with KSS at 3years of age. At 4years he presented with a cough and left upper lobe lung infiltrate as well as a hyperosmolar hyperglycemic episode. He subsequently required multiple daily insulin injections. This patient developed cardiomyopathy and died at the age of 10years. The second case was a 6-year-old boy of Asian ancestry who presented with ataxia exacerbated by intercurrent illnesses, decreased exercise tolerance, gross motor and fine motor delays, anorexia and recurrent episodes of vomiting associated with dehydration, and he was subsequently diagnosed with KSS. At 11years of age, the patient developed hyperosmolar hyperglycemia, and after treatment for it, he required multiple daily insulin injections. He died of end stage congestive heart failure secondary to cardiomyopathy at 13years of age. These 2 cases are presented to describe the possible pathophysiology of mitochondrial diabetes and to emphasize the need to monitor for the development of diabetes in patients with known mitochondrial disease and also to be aware of possible mitochondrial disease in pediatric patients who present with hyperglycemia in the context of multisystem involvement.

The use of FINDRISC questionnaire in assessment of risk of the type 2 diabetes development in patients with hypertension

The use of FINDRISC questionnaire in assessment of risk of the type 2 diabetes development in patients with hypertension

WS6.3 Subtle defects in glucose metabolism prior to development of diabetes in patients with cystic fibrosis

WS6.3 Subtle defects in glucose metabolism prior to development of diabetes in patients with cystic fibrosis

High-dose clevudine impairs mitochondrial function and glucose-stimulated insulin secretion in INS-1E cells

BackgroundClevudine is a nucleoside analog reverse transcriptase inhibitor that exhibits potent antiviral activity against hepatitis B virus (HBV) without serious side effects. However, mitochondrial myopathy has been observed in patients with chronic HBV infection taking clevudine. Moreover, the development of diabetes was recently reported in patients receiving long-term treatment with clevudine. In this study, we investigated the effects of clevudine on mitochondrial function and insulin release in a rat clonal β-cell line, INS-1E.MethodsThe mitochondrial DNA (mtDNA) copy number and the mRNA levels were measured by using quantitative PCR. MTT analysis, ATP/lactate measurements, and insulin assay were performed.ResultsBoth INS-1E cells and HepG2 cells, which originated from human hepatoma, showed dose-dependent decreases in mtDNA copy number and cytochrome c oxidase-1 (Cox-1) mRNA level following culture with clevudine (10 μM-1 mM) for 4 weeks. INS-1E cells treated with clevudine had reduced total mitochondrial activities, lower cytosolic ATP contents, enhanced lactate production, and more lipid accumulation. Insulin release in response to glucose application was markedly decreased in clevudine-treated INS-1E cells, which might be a consequence of mitochondrial dysfunction.ConclusionsOur data suggest that high-dose treatment with clevudine induces mitochondrial defects associated with mtDNA depletion and impairs glucose-stimulated insulin secretion in insulin-releasing cells. These findings partly explain the development of diabetes in patients receiving clevudine who might have a high susceptibility to mitochondrial toxicity.

Patients Newly Diagnosed with Clinical Type 2 Diabetes during Oral Glucocorticoid Treatment and Observed for 14 Years: All‐Cause Mortality and Clinical Developments

Chronic exposure to glucocorticoids (GCs) has many side effects including glucose intolerance and diabetes and may accelerate the occurrence of cardiovascular disease and increase mortality. We studied the 14-year clinical development of diabetes in patients diagnosed with diabetes during GC treatment. A population-based sample of 1369 people newly diagnosed with clinical type 2 diabetes underwent a clinical examination at diagnosis, and surviving patients were followed up 6 and 14 years later. Patients receiving oral GC treatment at diagnosis were compared with the other patients. Of 1369 patients, 35 (2.6%) were treated with oral GCs at diabetes diagnosis. At that point, patients on GC therapy were older (69.9 versus 65.3 years, p = 0.007, sex-adjusted) and tended to have lower BMI (26.1 versus 29.1 kg/m(2) , p = 0.023), also 6 years after diagnosis (24.8 versus 28.4, p = 0.011), than patients not being treated with GCs. In a univariate Cox regression model, GC treatment at diagnosis increased all-cause mortality with a hazard ratio (95% confidence interval) of 2.01 (1.39-2.89, p = 0.0002, n = 1369), while this decreased to 1.41 (0.98-2.04, p = 0.065, n = 1369) when adjusted for age and sex and to 1.39 (0.92-2.11, p = 0.12, n = 1086) when risk factors, complications and cancer were added to the model. Apart from differences in age and overweight, patients in this relatively small sample of those diagnosed with clinical type 2 diabetes during GC treatment were comparable at diagnosis and during 14 years of follow-up with those not treated with GCs, including with regard to the adjusted mortality rate.

Immunogenetic susceptibility to diabetes mellitus in patients with liver disease

Genetic, environmental, metabolic and infectious influences, such as hepatitis C virus (HCV) infection, are thought to impact on the development of diabetes in patients with liver disease. As specific human leucocyte antigen (HLA) alleles provide the major genetic risk factors for type 1 diabetes, our aim was to investigate whether HLA class I and II alleles constitute additional risk factors for diabetes in patients with liver disease. We evaluated two independent databases of 193 and 728 adult patients with chronic liver disease for the diagnosis of diabetes and the presence of specific HLA subtypes. In each database, 24 and 19% of patients met criteria for diabetes. In the first database, specific class I and II alleles were observed more frequently in diabetics compared with non-diabetics: Cw7 (50 vs. 32%, P=0.04), DR51 (17 vs. 3%P=0.003) and DQ6 (37 vs. 18%, P=0.02). In the second database, DQ6 was observed in 16% of diabetics vs. 8% of non-diabetics (P=0.04). The DR2-DR51-DQ6 haplotype was higher in patients with diabetes in both databases (22 vs.7%, P=0.02 and 12 vs. 5%, P=0.02). In a subgroup analysis of patients with HCV infection, increased frequencies of Cw7, DR2/DR51, DQ6 and DR2-DR51-DQ6 were also observed to be higher in subjects with diabetes compared with those without diabetes. Patients with chronic liver disease, especially those with HCV infection, have an immunogenetic risk for diabetes characterized by the presence of Cw7, DR51, DQ6 and DR2-DR51-DQ6.

Multivariate analysis of risk factors for the development of type 2 diabetes in nonalcoholic fatty liver disease

Diabetes is present in patients with nonalcoholic fatty liver disease (NAFLD). The aim of this retrospective cohort study was to assess the cumulative development of type 2 diabetes and predictive factors for its development in Japanese patients with NAFLD. A total of 6003 NAFLD patients diagnosed by ultrasonography were enrolled. The mean follow-up period was 4.9 years. An overnight (12 h) fasting blood sample or a casual blood sample was taken for routine analyses during follow up. The primary outcome was the development of type 2 diabetes. Evaluation was performed by using the Kaplan-Meier method and Cox proportional hazards analysis. Of the 6003 NAFLD patients, 411 patients developed type 2 diabetes. The cumulative development rate of type 2 diabetes was 6.8% at the 5th year and 17.7% at the 10th year. Multivariate Cox proportional hazards analysis showed that type 2 diabetes development in patients with NAFLD occurred when patients had prediabetes status (hazard ratio 6.39; 95% confidence interval 5.00-8.18; P < 0.001), mean serum gamma-glutamyltransferase (GGT) level of more than 109 IU/l (hazard ratio 1.60; 95% confidence interval 1.22-2. 02; P < 0.001), mean serum triglyceride (TG) level of more than 150 mg/l (hazard ratio 1.28; 95% confidence interval 1.05-1.55; P = 0.020), and physical activity of less than 60 min per week (hazard ratio 1.60; 95% confidence interval 1.25-2.00; P < 0.001). The improvement of prediabetes status and physical activity, and the normalization of mean GGT and TG levels during follow up are important to prevent the development of T2DM in patients with NAFLD.

Intensive therapy for diabetes through influence on innate immune system

Steno-2 Study has previously shown that original intensive therapy reduced the risk of cardiovascular and microvascular events to about 50% of that of conventional treatment in type 2 diabetic patients. Further, in the subsequent follow-up study, intensive therapy was found to have sustained beneficial effects on cardiovascular events and death rate in this population. Another clinical trial, China Da Qing Diabetes Prevention Study, has recently reported that group-based lifestyle interventions over six years could prevent or delay the development of diabetes in patients with impaired glucose tolerance (IGT). The two famous intervention trials have demonstrated a consistent salutary effect of intensive therapy on the development and progression of diabetes and its complications. However, the exact mechanisms of the sustained beneficial effects remain to be elusive. There is a growing body of evidence to suggest that type 2 diabetes is associated with a general activation of the innate immune system, in which there is a chronic, cytokine-mediated state of low-grade inflammation. Some diabetic treatment agents with anti-inflammatory properties may lower both acute-phase reactants which are components of the innate immune system independent of their anti-hyperglycemic actions or lipid-lowering effects. The immunomodulatory effects of regular exercise, and in particular resistance training, may have positive effects on innate immunity and so may provide benefits for the profile of type 2 diabetes in addition to improving strength and functional abilities. Therefore, we speculate that the effects on the innate immune system through pharmacologic therapy or lifestyle modification such as exercise training are able to account - at least amongst others - for carry-over beneficial effects of multifactorial intervention on insulin resistance and type 2 diabetes. This hypothesis, if proved to be valid, might provide a new therapeutic option for the management of type 2 diabetes.

Predictors of Development of Diabetes in Patients With Chronic Heart Failure in the Candesartan in Heart Failure Assessment of Reduction in Mortality and Morbidity (CHARM) Program

OBJECTIVEThe purpose of this study was to identify predictors of incident diabetes during follow-up of nondiabetic patients with chronic heart failure (CHF) in the Candesartan in Heart Failure Assessment of Reduction in Mortality and Morbidity (CHARM) program.RESEARCH DESIGN AND METHODSA total of 1,620 nondiabetic patients had full baseline datasets. We compared baseline demographic, medication, and laboratory data for patients who did or did not develop diabetes and conducted logistic regression and receiver operator characteristic curve analyses.RESULTSOver a median period of 2.8 years, 126 of the 1,620 patients (7.8%) developed diabetes. In multiple logistic regression analysis, the following baseline characteristics were independently associated with incident diabetes in decreasing order of significance by stepwise selection: higher A1C (odds ratio [OR] 1.78 per 1 SD increase; P < 0.0001), higher BMI (OR 1.64 per 1 SD increase; P < 0.0001), lipid-lowering therapy (OR 2.05; P = 0.0005), lower serum creatinine concentration (OR 0.68 per 1 SD increase; P = 0.0018), diuretic therapy (OR 4.81; P = 0.003), digoxin therapy (OR 1.65; P = 0.022), higher serum alanine aminotransferase concentration (OR 1.15 per 1 SD increase; P = 0.027), and lower age (OR 0.81 per 1 SD increase; P = 0.048). Using receiver operating characteristic curve analysis, A1C and BMI yielded areas under the curve of 0.723 and 0.712, respectively, increasing to 0.788 when combined. Addition of other variables independently associated with diabetes risk minimally improved prediction of diabetes.CONCLUSIONSIn nondiabetic patients with CHF in CHARM, A1C and BMI were the strongest predictors of the development of diabetes. Other minor predictors in part reflected CHF severity or drug-associated diabetes risk. Identifying patients with CHF at risk of diabetes through simple criteria appears possible and could enable targeted preventative measures.

Possible link of food-derived advanced glycation end products (AGEs) to the development of diabetes

China Da Qing diabetes prevention study has recently shown that group-based lifestyle interventions over six years can prevent or delay the development of diabetes in patients with impaired glucose tolerance (IGT) for up to 14 years after the active intervention. These findings suggest the sustained beneficial effects of lifestyle interventions to prevent diabetes in at-risk patients for diabetes. Therefore, the clinical study suggests that so-called 'metabolic memory' is involved in the development of diabetes. Potential mechanisms for propagating this 'metabolic memory' are the non-enzymatic glycation of proteins. The formation and accumulation of advanced glycation end products (AGEs) have been known to progress at an accelerated rate under diabetes, and there is accumulating evidence that AGEs play a role in the development of diabetes by inducing islet beta cell damage and/or insulin resistance. Further, there are several animal studies to suggest that dietary AGEs are involved in insulin resistance, visceral obesity and the development of diabetes. These findings led us to speculate that the long-term beneficial influence of early lifestyle interventions on the development of diabetes could be ascribed, at least in part, to their inhibitory effects on AGEs. That is, intake of food-derived AGEs may be suppressed in the lifestyle intervention group, which could reduce the risk for the development of diabetes in high-risk patients with IGT. Therefore, it is an interesting issue to clarify whether food-derived AGEs are actually restricted during the active intervention period and if circulating or tissue AGE levels at the closure of the China Da Qing diabetes prevention study could predict the risk for the development of diabetes 14 years after the trial. This additional, clinical investigation may provide us more information about whether restriction of food-derived AGEs is beneficial for the prevention of the development of diabetes in high-risk patients and may be a novel therapeutic target to prevent diabetes and its related complications.

Impact of Diabetes on the Severity of Liver Disease

The prevalence of type 2 diabetes is higher in patients who have liver diseases, such as nonalcoholic fatty liver disease, chronic viral hepatitis, hemochromatosis, alcoholic liver disease, and cirrhosis. The development of diabetes in patients with cirrhosis is well recognized, but evidence is emerging that the development of chronic liver disease and progression to cirrhosis may occur after the diagnosis of diabetes and that diabetes plays a role in the initiation and progression of liver injury. This article provides an overview of the evidence for an increased prevalence of diabetes in a range of liver diseases; the effect of diabetes on the severity of disease; the potential mechanisms whereby coexistent diabetes exacerbates progression of hepatic fibrosis; and the impact of obesity, insulin resistance, and type 2 diabetes on clinical outcomes.

Is vitamin E beneficial in chronic liver disease?

The prevalence of type 2 diabetes is higher in patients who have liver diseases, such as nonalcoholic fatty liver disease, chronic viral hepatitis, hemochromatosis, alcoholic liver disease, and cirrhosis. The development of diabetes in patients with cirrhosis is well recognized, but evidence is emerging that the development of chronic liver disease and progression to cirrhosis may occur after the diagnosis of diabetes and that diabetes plays a role in the initiation and progression of liver injury. This article provides an overview of the evidence for an increased prevalence of diabetes in a range of liver diseases; the effect of diabetes on the severity of disease; the potential mechanisms whereby coexistent diabetes exacerbates progression of hepatic fibrosis; and the impact of obesity, insulin resistance, and type 2 diabetes on clinical outcomes.

High-Sensitivity C-Reactive Protein as Cardiovascular Risk Marker in Patients with Diabetes Mellitus

C-reactive protein (CRP) is a liver-derived pattern recognition molecule that is increased in inflammatory states. It rapidly increases within hours after tissue injury, and it is suggested that it is part of the innate immune system and contributes to host defense. Since cardiovascular disease is at least in part an inflammatory process, CRP has been investigated in the context of arteriosclerosis and subsequent vascular disorders. Based on multiple epidemiological and intervention studies, minor CRP elevation [high-sensitivity CRP (hsCRP)] has been shown to be associated with future major cardiovascular risk (hsCRP:<1 mg/L=low risk; 1-3 mg/L=intermediate risk; 3-10 mg/L=high risk; >10 mg/L=unspecific elevation). It is recommended by the American Heart Association that patients at intermediate or high risk of coronary heart disease may benefit from measurement of hsCRP with regard to their individual risk prediction. Elevation of hsCRP is associated with increased risk of type 2 diabetes development in patients with all levels of metabolic syndrome. In type 1 and type 2 diabetes mellitus, hemoglobin A1c significantly correlates with hsCRP levels and future cardiovascular risk. Also, hsCRP levels increase with the stage of beta-cell dysfunction and insulin resistance. Non-diabetes drugs that have been shown to reduce hsCRP concentrations include aspirin, statins, cyclooxygenase-2 inhibitors, and fibrates. Recent intervention studies have also demonstrated the distinct efficacy of different anti-diabetes treatments on a variety of cardiovascular risk markers. Intensive insulin therapy may reduce inflammation, but this effect may be influenced by the degree of weight gain. Treatment with peroxisome proliferator-activated receptor gamma has lead to substantial reduction of hsCRP and other cardiovascular risk markers in several comparator studies. Since this effect was shown to be independent of the degree of glycemic improvement, it can be regarded as a classspecific effect. Whether these findings translate into a reduction of overall cardiovascular mortality will soon be shown by the currently running thiazolidinedione outcome studies. Positive results in these trials will further strengthen the value and acceptance of hsCRP, which is recommended as a predictive laboratory marker for cardiovascular disease risk also in patients with diabetes mellitus.

Adiponectin and the development of diabetes in patients with coronary artery disease and impaired fasting glucose

Adiponectin has insulin-sensitizing properties, and high adiponectin levels have been shown to be associated with reduced risk of developing diabetes. Patients with coronary artery disease (CAD) have relatively low adiponectin levels and high prevalence of glucose intolerance. The role of adiponectin in predicting the development of diabetes in this high-risk group has not been determined. The study aimed to determine whether baseline adiponectin levels predict the development of diabetes in a group of patients with CAD and impaired fasting glucose (IFG). A total of 588 patients who participated in the Bezafibrate Infarction Prevention (BIP) study and who had at baseline fasting glucose of 100-125 mg/dl were included and followed for 6.2+/-1.3 years. Adiponectin was determined in frozen plasma samples taken at baseline. Of the patients with IFG at baseline, 256 (44%) developed diabetes during follow-up. The patients who developed diabetes had at baseline higher body-mass index, fasting glucose, C-reactive protein, triglycerides, homeostatic assessment of insulin resistance (HOMA-IR) and diastolic blood pressure than patients who did not develop diabetes. Adiponectin levels at baseline were significantly lower in patients who developed diabetes than in patients who did not develop diabetes (P = 0.009, nonparametric Kruskall-Wallis test). An increase of 1 unit of natural logarithm of adiponectin level was associated with a hazard ratio of 0.77 (95% CI, 0.61-0.96) for diabetes development. Patients with CAD and IFG have a very high rate of conversion to type 2 diabetes. Even in this high-risk group, high adiponectin levels are associated with reduced risk of developing diabetes.

Insulin secretory defect plays a major role in the development of diabetes in patients with distal pancreatectomy

To investigate the pathogenesis of distal pancreatectomy (d-Px)–induced diabetes in Korean patients, we investigated insulin secretory and sensitivity indexes obtained by oral glucose tolerance testing in 20 patients that had received d-Px (10 with d-Px–induced diabetes and 10 with normal glucose tolerance with d-Px [NGT d-Px]) and in 164 control subjects (77 with type 2 diabetes mellitus and 87 with NGT) that did not receive d-Px. The pancreatectomized subjects had lower fasting serum insulin, homeostasis model assessment of pancreatic beta-cell function (HOMA- β) levels, and insulinogenic indices than the NGT controls. The HOMA- β values of nonobese NGT d-Px– and d-Px–induced diabetic subjects were 73.7% and 38.7% of those for nonobese NGT controls, respectively, and HOMA- β was significantly lower only for d-Px–induced diabetic subjects ( P < .01). In obese subjects, the HOMA- β values of obese d-Px–induced diabetic subjects were significantly lower than those of obese NGT controls ( P < .05). The insulin sensitivity was significantly lower in nonobese type 2 diabetes mellitus controls than in nonobese NGT d-Px or in nonobese d-Px–induced diabetic subjects ( P < .001 and .05, respectively). These results show that a reduced insulin secretory function is a typical feature of glucose homeostasis in distal pancreatectomized patients and that insulin secretory defect plays a major role in the development of diabetes in these patients. In addition, the study suggests that pancreatic resections of 60% or less and body mass index are not the main causes of diabetes onset after d-Px in this study.

Diet, diabetes and schizophrenia: review and hypothesis.

Diabetes is more common in people with schizophrenia than in the general population. To explore the possible reasons for the association between diabetes and schizophrenia. Diet and other lifestyle factors in patients with schizophrenia were reviewed as risk factors for diabetes. People with schizophrenia show features of the metabolic syndrome at the onset of illness, before treatment. They also eat a poor diet, take little exercise and have high rates of smoking. Food intake may be increased further by antipsychotic medication. Nutritional factors appear to have a key role in the development of diabetes in patients with schizophrenia and may also affect the outcome and severity of schizophrenia. A common pathway through which diet might contribute to the development of both diabetes and schizophrenia is proposed. Lifestyle factors may influence outcomes in both diabetes and schizophrenia. Lifestyle interventions are the key to improving the long-term health of people with schizophrenia.