Elevated Fasting Glucose Levels Research Articles

Cardiovascular Risk in Patients With Fasting Blood Glucose Levels Within Normal Range

Fasting glucose levels elevated beyond the normal range have been associated with increased cardiovascular risk. However, it is unknown whether this association exists for variations of fasting glucose within the normal range. The present study was conducted using the computerized database of the Sharon-Shomron District of Clalit Health Services. Included in the present study were subjects with fasting glucose levels within the normal range (< 100 mg/dl). We excluded patients with a history of cardiovascular disease or diabetes. The primary outcome was the incidence of coronary revascularization with either percutaneous coronary intervention or coronary artery bypass grafting. The 28,263 participants (age 53.7 ± 12.2 years) were divided into quartiles according to the fasting glucose level (75.4 ± 4.5, 83.6 ± 1.7, 88.9 ± 1.4, and 95.1 ± 2.2 mg/dl). During a mean follow-up of 5.9 ± 0.7 years, 424 subjects required coronary revascularization. A progressive increase was seen in the risk of coronary revascularization as the fasting glucose levels increased within the normal range (hazard ratio 1.73, 95% confidence interval 1.3 to 2.3, p > 0.001, between the fourth and first quartiles). However, this association lost its statistical significance after adjustments for the conventional coronary risk factors (hazard ratio 1.17, 95% confidence interval 0.85 to 1.62, p = 0.328). In conclusion, elevated fasting glucose levels within the normal range were associated with an increased cardiovascular risk. This association was caused by the greater prevalence of the other conventional risk factors and not by the glucose level itself.

Lymphatic system: a vital link between metabolic syndrome and inflammation

Metabolic syndrome is defined by a cluster of different metabolic risk factors that include overall and central obesity, elevated fasting glucose levels, dyslipidemia, hypertension, and intimal atherogenesis. Metabolic syndrome leads to increased risk for the development of type 2 diabetes and cardiovascular disease (e.g., heart disease and stroke). The exacerbated progression of metabolic syndrome to cardiovascular disease has lead to intense study of the physiological ramifications of metabolic syndrome on the blood vasculature. These studies have particularly focused on the signaling and architectural alterations that manifest in hypertension and atherosclerosis. However, despite the overlap of metabolic syndrome pathology with lymphatic function, tangent effects on the lymphatic system have not been extensively documented. In this review, we discuss the current status of metabolic syndrome and provide evidence for, and the remaining challenges in studying, the connections among the lymphatic system, lipid transport, obesity, insulin resistance, and general inflammation.

Chronic social defeat stress disrupts regulation of lipid synthesis

Several psychiatric disorders increase the risk of cardiovascular disease, including posttraumatic stress disorder and major depression. While the precise mechanism for this association has not yet been established, it has been shown that certain disorders promote an unfavorable lipid profile. To study the interaction of stress and lipid dysregulation, we utilized chronic social defeat stress (CSDS), a mouse model of chronic stress with features of posttraumatic stress disorder and major depression. Following exposure to CSDS, mice were given access to either regular chow or a Western-style diet high in fat and cholesterol (HFD). The combination of social stress and HFD resulted in significant perturbations in lipid regulation, including two key features of the metabolic syndrome: increased plasma levels of non-HDL cholesterol and intrahepatic accumulation of triglycerides. These effects were accompanied by a number of changes in the expression of hepatic genes involved in lipid regulation. Transcriptional activity of LXR, SREBP1c, and ChREBP were significantly affected by exposure to HFD and CSDS. We present CSDS as a model of social stress induced lipid dysregulation and propose that social stress alters lipid metabolism by increasing transcriptional activity of genes involved in lipid synthesis.

Pericardial adipose tissue, atherosclerosis, and cardiovascular disease risk factors: the Jackson heart study.

OBJECTIVEPericardial adipose tissue (PAT), a regional fat depot that surrounds the heart, is associated with an unfavorable cardiometabolic risk factor profile. The associations among PAT, cardiometabolic risk factors, and coronary artery calcification (CAC) and abdominal aortic artery calcification (AAC) in African American populations have not been explored.RESEARCH DESIGN AND METHODSA total of 1,414 African Americans (35% men; mean ± SD age 58 ± 11 years) drawn from the Jackson Heart Study (JHS) underwent multidetector computed tomography assessment of abdominal visceral adipose tissue (VAT) and PAT between 2007 and 2009. Cardiometabolic risk factors, CAC, and AAC were examined in relation to increments of PAT and VAT.RESULTSPAT was significantly correlated with BMI, waist circumference, and VAT (r = 0.35, 0.46, and 0.69; all P < 0.0001). PAT (per 1-SD increase) was associated with elevated levels of systolic blood pressure (P < 0.04), fasting glucose, triglycerides, and C-reactive protein and lower levels of HDL (all P values<0.0001). PAT was also associated with metabolic syndrome (odds ratio [OR] 1.89; P < 0.0001), hypertension (1.48; P < 0.0006), and diabetes (1.40; P < 0.04); all associations were diminished after further adjustment for VAT (most P > 0.05). However, the association of PAT with CAC but not with AAC remained significant (OR 1.34 [95% CI 1.10–1.64]; P < 0.004) after multivariable and VAT adjustment.CONCLUSIONSPAT is significantly correlated with most cardiometabolic risk factors and CAC in the JHS cohort. The results suggest that PAT is an important VAT depot that may exert a local effect on the coronary vasculature.

A Prospective Analysis of Elevated Fasting Glucose Levels and Cognitive Function in Older People

OBJECTIVETo investigate the relationship between fasting glucose levels, insulin resistance, and cognitive impairment in old age. Diabetes is associated with cognitive impairment in older people. However, the link between elevated fasting glucose levels and insulin resistance in nondiabetic individuals, and the risk of cognitive impairment is unclear.RESEARCH DESIGN AND METHODSWe analyzed data from, in total, 8,447 participants in two independent prospective studies: the PROspective Study of Pravastatin in the Elderly at Risk (PROSPER), 5,019 participants, aged 69–84 years, and the Rotterdam Study, 3,428 participants, aged 61–97 years. Fasting glucose levels were assessed at baseline in both studies; fasting insulin levels were assessed in the Rotterdam Study only. Cognitive function was assessed in both studies at baseline and during follow-up.RESULTSSubjects with diabetes had impaired cognitive function at baseline. In contrast, in people without a history of diabetes, there was no clear association between baseline fasting glucose levels and executive function and memory, nor was there a consistent relationship between elevated baseline fasting glucose levels and the rate of cognitive decline in either cohort. Insulin resistance (homeostasis model assessment index) was also unrelated to cognitive function and decline.CONCLUSIONSElevated fasting glucose levels and insulin resistance are not associated with worse cognitive function in older people without a history of diabetes. These data suggest either that there is a threshold for effects of dysglycemia on cognitive function or that factors other than hyperglycemia contribute to cognitive impairment in individuals with frank diabetes.

Metabolic syndrome predicts the incidence of hepatic steatosis in Koreans

It has not been well elucidated whether the development of metabolic syndrome and its components predicts the incidence of hepatic steatosis. A cohort of 1705 apparently healthy Korean adults (954 men and 751 women, 43.6 ± 8.5 years old) without ultrasonographically defined hepatic steatosis and with normal serum gamma-glutamyl-transpeptidase and alanine aminotransferase was followed from 2004 to 2007. Metabolic syndrome was defined as the presence of at least three of the following components: obesity (BMI ≥ 25.0 kg/m(2)), high blood pressure, elevated levels of triglycerides and fasting glucose, and low level of high-density lipoprotein cholesterol. The outcome was ultrasonographically diagnosed hepatic steatosis. The analyses were conducted using the Cox proportional hazards model and time-dependent Cox model. A total of 226 individuals developed hepatic steatosis during 3716 person-years of follow-up. The presence of one to two metabolic syndrome components at baseline significantly predicted the development of hepatic steatosis. Metabolic syndrome itself, having ≥1 metabolic syndrome components, and maintenance of metabolic syndrome during follow-up significantly increased the risk (hazard ratio 2.0-4.1 for men, 3.4-10.8 for women) after adjustment for the follow-up period, age and BMI at baseline or updated during follow-up. Occurrence of obesity, high triglycerides or high fasting glucose during follow-up significantly predicted the development of hepatic steatosis, even after adjustment for metabolic syndrome components at baseline. The presence at baseline and the development of metabolic syndrome during follow-up were risk factors for ultrasonographically detected hepatic steatosis.

Effect of Growth Hormone (GH) on Fasting and Postprandial Metabolism in GH Deficiency

Hypopituitarism with adult-onset growth hormone deficiency (GHD) is associated with increased cardiovascular morbidity and mortality due to premature and progressive atherosclerosis. An underlying cause of atherosclerosis is increased insulin resistance. Elevated fasting and postprandial glucose and lipid levels may contribute to premature atherosclerosis. We studied effects of growth hormone replacement (GHRT) on fasting and postprandial metabolic parameters as well as on insulin sensitivity in patients with adult-onset GHD. Using a standardized mixed meal, we studied insulin, glucose, non-esterified free fatty acid (NEFA) and triglycerides (TG) concentrations in the fasting state and during a 4 h postprandial period in 15 patients with adult-onset GHD before and after 4 months of GHRT. Identical investigations were performed in healthy matched control subjects. GHD patients before and after GHRT: GHRT did not result in significant changes in fasting glucose, insulin, NEFA and TG concentrations. In the postprandial period GHRT resulted in a non-significant increase in glucose and a decrease in NEFA levels in the presence of unchanged postprandial insulin and TG concentrations. GHD patients vs. control subjects: GHD patients showed similar fasting glucose, insulin and NEFA concentrations, but TG were increased. In the postprandial period GHD patients exhibited similar glucose and TG, but increased insulin and NEFA concentrations. GHRT patients vs. control subjects: Patients after GHRT had similar fasting glucose, insulin and NEFA, but increased TG concentrations. In the postprandial period patients after GHRT had increased glucose and insulin levels in the presence of similar NEFA and TG concentrations. While impaired insulin action in patients with GHD translates mainly by an impaired fasting TG metabolism, GHRT induced insulin resistance additionally encompasses postprandial glucose metabolism.

Investigation Into the Cardiac Effects of Spironolactone in the Experimental Model of Type 1 Diabetes

We have studied the effect of 8-week treatment with spironolactone (20 mg*kg(-1)*day(-1)) on cardiovascular complications associated with streptozotocin (STZ)-diabetic rats. Wistar rats were made diabetic with STZ (45 mg/kg, intravenously). Various biochemical and cardiac parameters were measured at the end of 8 weeks. STZ produced hyperglycemia; hypoinsulinemia; hyperlipidemia; increased blood pressure; increased creatinine, cardiac enzyme, and C-reactive protein levels; reduction in heart rate; and cardiac hypertrophy. Chronic treatment with spironolactone significantly prevented STZ-induced bradycardia, hypertension, and elevated fasting glucose level with simultaneous increase in serum insulin levels. It significantly reduced the elevated cholesterol, very-low-density lipoprotein, and triglyceride levels and increased the lower high-density lipoprotein-cholesterol levels in diabetic rats. Furthermore, spironolactone also produced a significant reduction in the elevated creatinine levels, C-reactive protein, and levels of lactate dehydrogenase and creatinine kinase. It also produced beneficial effect in diabetic rats by preventing cardiac hypertrophy as evident from decrease in left ventricular collagen levels, cardiac hypertrophy index, and left ventricular hypertrophy index. Our data suggest that spironolactone prevents not only the STZ-induced metabolic abnormalities but also cardiovascular complications.

Akt2 Is Required for Hepatic Lipid Accumulation in Models of Insulin Resistance

Insulin drives the global anabolic response to nutrient ingestion, regulating both carbohydrate and lipid metabolism. Previous studies have demonstrated that Akt2/protein kinase B is critical to insulin's control of glucose metabolism, but its role in lipid metabolism has remained controversial. Here, we show that Akt2 is required for hepatic lipid accumulation in obese, insulin-resistant states induced by either leptin deficiency or high-fat diet feeding. Lep(ob/ob) mice lacking hepatic Akt2 failed to amass triglycerides in their livers, associated with and most likely due to a decrease in lipogenic gene expression and de novo lipogenesis. However, Akt2 is also required for steatotic pathways unrelated to fatty acid synthesis, as mice fed high-fat diet had reduced liver triglycerides in the absence of hepatic Akt2 but did not exhibit changes in lipogenesis. These data demonstrate that Akt2 is a requisite component of the insulin-dependent regulation of lipid metabolism during insulin resistance.

Comparison of Cardiometabolic Syndrome Parameters, Obesity, Insulin Resistance, and Elevated Alanine Aminotransferase in Current Professional Baseball and Football Players

Purpose: Media news reports have suggested that professional football players (PFP) were twice as likely to die before the age of 50 as professional baseball players (PBP). To scientifically study this premise, we compared cardiometabolic syndrome parameters between PFP and PBP. Methods: Cardiometabolic syndrome markers [blood pressure (BP) ≥130/85 mmHg, fasting glucose (FG) ≥100 mg/dL, triglycerides (TG) ≥150 mg/dL, waist circumference (WC) ≥100 cm, high density lipoprotein (HDL) cholesterol ≤40 mg/dL] body mass index (BMI), parameters of obesity [BMI >30 mg/kg2, WC ≥100 cm, waist-to-height ratio (WHR) >0.5], insulin resistance [triglycerides/HDL (TG/HDL) >3.5], and elevated alanine aminotransferase (ALT) ≥40 IU/L were compared in 69 PFP to 155 PBP who gave written consent to participate. ALT ≥40 IU/L was chosen as the upper limit of normal as this was the value used in men aged 20-29 in the standard National Health and Nutrition Examination Study (NHANES III). Institutional review board approval was obtained. SAS 9.1 was used for statistical analysis, with a p value of significance defined as ≤0.05. Results: Comparing the study population of PFP to PBP, PFP have an increased FG >100 mg/dL, increased BMI >30 kg/m2, increased WC ≥100 cm, and increased WHR >0.5, but decreased BP ≥130/85. In the subset of 19 Linemen (guards, tackles, centers, and defensive ends) compared to PBP, there was a significant increase in FG ≥100 mg/dL, BMI >30 kg/m2, WC ≥100 cm, WHR >0.5, and an increased incidence of the cardiometabolic syndrome (≥3 of the markers). There was no difference in BP between linemen and PBP. In the subset of 50 non-linemen (all other PFP other than linemen) compared to PBP, there was a significant increase in BMI but a significant decrease in BP and ALT. There was no difference in FG ≥ 100 mg/dl between non-linemen and PBP. Conclusion: PFP have increased obesity markers and hyperglycemia compared to PBP. However, elevated fasting glucose levels, obesity (as measured by WC and WHR), and increased cardiometabolic syndrome incidence in PFP were confined to the linemen subset. PBP have increased hypertension compared to PFP, the etiology of which is unclear. The increased cardiometabolic markers and implied cardiovascular risk for PFP appears to be limited to the linemen subset.

Metabolic Syndrome Is Associated With Venous Thromboembolism in the Korean Population

The metabolic syndrome (MS) is a known risk factor for arterial thromboembolism. Preliminary reports have also suggested the association between MS and venous thromboembolism (VTE). In this case-control study, we investigated the association between MS and VTE in Korean patients. Patients with objectively diagnosed VTE and healthy control subjects underwent clinical assessment for the presence of MS according to the National Cholesterol Education Adult Treatment Panel III criteria modified with body mass index (WHO Asian Pacific Perspective, 2000). The presence of known risk factors for VTE was ascertained. Patients with VTE secondary to cancer were excluded. The prevalence of MS was compared between VTE group and controls. Two hundred eight VTE patients and 300 controls were assessed. VTE was idiopathic in 91 patients and secondary to a known risk factor in 117. The prevalence of MS was significantly higher in VTE patients (47.6%) than in controls (37.7%) (OR: 1.50; 95% CI: 1.05 to 2.15, P=0.026). After adjusting for age, sex, and smoking status, metabolic MS remained independently associated with VTE (OR: 1.56; 95% CI: 1.07 to 2.27, P=0.020). In the subgroup analysis, MS was also independently associated with idiopathic VTE (OR: 1.71; 95% CI: 1.04 to 2.81, P=0.033), but not with secondary VTE (OR: 1.43; 95% CI: 0.91 to 2.99, P=0.121). Multivariate analysis demonstrated that high BMI (OR: 1.70, 95% CI: 1.01 to 2.87), decreased HDL cholesterol (OR: 1.99, 95% CI: 1.17 to 3.39), and elevated fasting glucose levels (OR: 2.31; 95% CI: 1.35 to 3.94) were associated with idiopathic VTE. MS is associated with VTE and in particular with idiopathic VTE in the Korean population.

NECROLYTIC MIGRATORY ERYTHAEMA AND GLUCAGONOMA SYNDROME

A 52-year old woman presented with vomiting, vague abdominal pain, progressive weight loss (85 kg to 76 kg) over the past 6 months and recurrent skin eruptions on her face, perineum and the extremities (fi gure A,B,C) which were diagnosed and treated as eczema. First evaluation revealed elevated fasting glucose level (139 mg/dl normal value 60-105) and oesophagogastroduodenoscopy showed refl ux oesophagitis grade A. CT scan and MRI of the abdomen showed a nodular hypervascular mass of 6,5 cm in the tail of the pancreas with lymph node involvement and multiple liver metastases (fi gure D). Other laboratory testing revealed markedly elevated glucagon (2970 pg/ml, normal value < 250), chromogranin A (517 μg/l, normal value 40-70). Diagnosis of a glucagonoma syndrome with necrolytic migratory erythema (NME) was made. Octreotide LAR, 20 mg once monthly was started. She underwent resection of the pancreatic tail and splenectomy. Three months later she underwent two sessions of transarterial doxorubicin based chemoembolisation of the liver, with stabilisation of her disease. She is still in follow-up with three monthly evaluations. Glucagonoma syndrome is a rare malignant disorder of the pancreas tumour, which comprises hyperglucagonaemia, diabetes mellitus, anaemia, weight loss, fatigue and NME. The incidence is 1 in 20 million per year. Dermatologic changes in NME may be misdiagnosed as they can suggest other dermatoses. The pathogenesis of NME remains controversial. Improvement in NME is often seen after surgery, somatostatin analogues and after supplementation. Spiral CT is the initial imaging procedure of choice. The optimal treatment for glucagonoma is dependent on the stage of the tumour and

Selective mtDNA mutation accumulation results in β-cell apoptosis and diabetes development

To test the hypothesis that somatic mitochondrial (mt)DNA mutation accumulation predisposes mice to beta-cell loss and diabetes development, transgenic mice expressing a proofreading-deficient mtDNA polymerase-gamma under the control of the rat insulin-1 promoter were generated. At 6 wk of age, mtDNA mutations reached 0.01% (1.05 mutations/10,000 bp) in islets isolated from transgenic mice. This mutational burden is associated with impaired glucose tolerance and a diabetes prevalence of 52% in male transgenic mice. Female transgenic mice maintain slightly elevated fasting glucose levels, mild glucose intolerance, and a diabetes prevalence of 14%. Diabetes in transgenic animals is associated with insulin insufficiency that results from a significant reduction in beta-cell mass. Importantly, apoptosis of beta-cells is increased 7-fold in female and 11-fold in male transgenic mice compared with littermate controls. These results are consistent with a causative role of somatic mtDNA mutation accumulation in the loss of beta-cell mass and diabetes development.

Genetic factors for resistance to diet-induced obesity and associated metabolic traits on mouse chromosome 17.

Obesity is associated with increased susceptibility to dyslipidemia, insulin resistance, and hypertension, a combination of traits that comprise the traditional definition of the metabolic syndrome. Recent evidence suggests that obesity is also associated with the development of nonalcoholic fatty liver disease (NAFLD). Despite the high prevalence of obesity and its related conditions, their etiologies and pathophysiology remains unknown. Both genetic and environmental factors contribute to the development of obesity and NAFLD. Previous genetic analysis of high-fat, diet-induced obesity in C57BL/6J (B6) and A/J male mice using a panel of B6-Chr(A/J)/NaJ chromosome substitution strains (CSSs) demonstrated that 17 CSSs conferred resistance to high-fat, diet-induced obesity. One of these CSS strains, CSS-17, which is homosomic for A/J-derived chromosome 17, was analyzed further and found to be resistant to diet-induced steatosis. In the current study we generated seven congenic strains derived from CCS-17, fed them either a high-fat, simple-carbohydrate (HFSC) or low-fat, simple-carbohydrate (LFSC) diet for 16 weeks and then analyzed body weight and related traits. From this study we identified several quantitative trait loci (QTLs). On a HFSC diet, Obrq13 protects against diet-induced obesity, steatosis, and elevated fasting insulin and glucose levels. On the LFSC diet, Obrq13 confers lower hepatic triglycerides, suggesting that this QTL regulates liver triglycerides regardless of diet. Obrq15 protects against diet-induced obesity and steatosis on the HFSC diet, and Obrq14 confers increased final body weight and results in steatosis and insulin resistance on the HFSC diet. In addition, on the LFSC diet, Obrq 16 confers decreased hepatic triglycerides and Obrq17 confers lower plasma triglycerides on the LFSC diet. These congenic strains provide mouse models to identify genes and metabolic pathways that are involved in the development of NAFLD and aspects of diet-induced metabolic syndrome.

Current strategies for the inhibition of hepatic glucose production in type 2 diabetes

Diabetes is a complex disease involving multiple organs with dysregulation in glucose and lipid metabolism. Hepatic insulin insensitivity can contribute to elevated fasting glucose levels and impaired glucose tolerance in individuals with diabetes. Several currently available therapeutics address defects at the liver. Metformin inhibits glucose production, potentially through effects on AMPK. Thiazolidinediones activate PPAR-gamma and improve hepatic insulin sensitivity, primarily through indirect effects on lipid metabolism. Insulin analogs and secretagogues suppress glucose production and increase liver glucose utilization by both direct and indirect hepatic actions. Incretins, incretin mimetics, and dipeptidyl peptidase-4 inhibitors reduce postprandial hepatic glucose production by increasing insulin secretion and limiting glucagon release, as well as through possible direct effects on the liver. Pramlintide reduces the increase in plasma glucagon that occurs following a meal in individuals with diabetes, and may thereby suppress inappropriate stimulation of liver glucose production. Many other hepatic targets are being considered which may lead to alternative strategies for the treatment of diabetes. This review focuses on currently available therapeutics which target insulin resistance in the liver.

The Obese Without Cardiometabolic Risk Factor Clustering and the Normal Weight With Cardiometabolic Risk Factor Clustering Prevalence and Correlates of 2 Phenotypes Among the US Population (NHANES 1999–2004)

The individual risk of cardiovascular disease (CVD) may depend on both body size and the metabolic profile. Individuals with a similar body mass index (BMI) may express a different clustering of cardiometabolic risk factors (variable body size phenotypes). There are few data regarding the prevalence and correlates of two body size phenotypes, one, a subset of normal-weight individuals displaying cardiometabolic risk factor clustering, and the other a subset of obese individuals resistant to the development of the adiposity-associated cardiometabolic abnormalities. These parameters were examined in an observational study involving 5440 participants of the National Health and Nutrition Examination Surveys (NHANES) 1999-2004 database who were 20 years of age and older. Individuals were classified according to their BMI as either normal weight, <25.0; overweight, 25.0-29.9; and obese, ≥30.0 [calculated as weight in kilograms divided by height in meters squared]. The cardiometabolic abnormalities include elevated blood pressure and insulin resistance; elevated levels of triglycerides, fasting glucose, and C-reactive protein; and reduced level of high density lipoprotein cholesterol (HDL-C). The metabolically healthy phenotype is defined as ≤2 metabolic abnormalities and the metabolically abnormal as ≥3 metabolic abnormalities. Each of 6 body size phenotypes were evaluated: normal-weight, overweight, and obese individuals with or without cardiometabolic abnormalities. A multivariate adjustment regression model was used to calculate the independent risk factors for CVD. The data show that, of the phenotypes expressed as percentage of each BMI group, 51.3% (approximately 35.9 million adults) of overweight adults and 31.7% (approximately 19.5 million adults) of obese adults were metabolically healthy, whereas 23.5% (approximately 16.3 million adults) of normal-weight adults were metabolically abnormal. Among normal-weight individuals, risk factors independently associated with the metabolically abnormal phenotype were older age, larger waist circumference, and lower physical activity. Among overweight and obese individuals, independent risk factors for expression of the metabolically healthy phenotype were younger age, smaller waist circumference, higher physical activity, and non-Hispanic black race/ethnicity. These findings indicate that among US adults there is a high prevalence of overweight and obese individuals who are metabolically healthy, and a high prevalence of normal-weight individuals who express a clustering of cardiometabolic abnormalities.

Metabolic consequences of a 50% partial pancreatectomy in humans

Partial pancreatectomy is frequently performed in patients with pancreatic tumours or chronic pancreatitis, but little is known about the metabolic impact of this intervention. We examined the effects of approximately 50% partial pancreatectomy on glucose homeostasis and insulin secretion. Fourteen patients with chronic pancreatitis, ten patients with pancreatic carcinoma and 13 patients with benign pancreatic tumours or extra-pancreatic masses (control group) underwent 240 min oral glucose tolerance tests before and after pancreatic tail-resection (n = 12), duodenopancreatectomy (n = 19) or duodenum-preserving pancreatic-head resection (n = 6). Partial pancreatectomy led to a reduction in post-challenge insulin excursions by 49% in chronic pancreatitis patients, 52% in carcinoma patients and 55% in controls (p < 0.05). Nevertheless, post-challenge glucose concentrations were transiently ameliorated after surgery (p < 0.001). In the control participants, pancreatic-head resection caused a transient reduction of post-challenge glycaemia, whereas pancreatic-tail resection increased both fasting and post-challenge glycaemia (p < 0.05). Insulin sensitivity was highest in chronic pancreatitis patients before surgery (p < 0.01), but remained unchanged by the partial pancreatectomy. High pre-operative body weight and elevated fasting glucose levels were associated with poor glycaemic control after surgery. Insulin secretion is diminished after pancreatic-head and -tail resection, but post-challenge glucose concentrations can be ameliorated after pancreatic-head resection. These data highlight the unequal impact of different surgical procedures on glucose control and suggest that obesity and high pre-operative glucose levels should be considered as risk factors for the development of hyperglycaemia after pancreatic surgery.

Glucose homeostasis abnormalities in cardiac intensive care unit patients

The aim of this study was to characterize the abnormalities in glucose homeostasis in intensive care unit patients following an acute coronary event. The study population included all non-diabetic patients ages 20-80 years that were admitted to a coronary intensive unit. Glucose, insulin and C-peptide levels during an oral glucose tolerance test (OGTT) were measured during the acute admission. From January to September 2003, 277 patients were admitted to the coronary unit. Of these, 127 patients underwent an OGTT. Of these, only 29 patients (23%) exhibited normal glucose metabolism. The remainder had type 2 diabetes (32%), impaired glucose tolerance (37%) or isolated impaired fasting glucose (8%, 100-125 mg/dl). Based on homeostasis model assessment (HOMA) calculations, diabetic patients had impaired beta-cell function and patients with elevated fasting glucose levels were insulin resistant. Beta-cell dysfunction during the acute stress seems to contribute to the glucose abnormalities. Most patients who experience an acute coronary event demonstrate abnormal glucose metabolism. Post glucose-load abnormalities are more common than abnormal fasting glucose level in this situation. It is postulated that the acute stress of a coronary event may contribute to the dysglycemia.

Metabolic syndrome in carbon disulfide-poisoned subjects in Korea: does chemical poisoning induce metabolic syndrome?

Mass carbon disulfide (CS(2)) poisoning was reported at a viscose rayon factory in Korea. We evaluated the association between CS(2) poisoning and the prevalence of metabolic syndrome. The cases (n = 170) involved CS(2)-poisoned subjects, who participated in a health examination conducted at a hospital in Korea in 2005. The controls (n = 170) were selected randomly from the participants in the third Korean National Health and Nutrition Examination Survey. Metabolic syndrome was defined as having at least three of following metabolic abnormalities: abdominal obesity, elevated triglyceride, reduced high-density lipoprotein cholesterol, elevated blood pressure, and elevated fasting glucose levels. After adjusting for covariates (age, gender, education, marital status, alcohol consumption, and smoking), CS(2)-poisoned subjects had an increased risk of metabolic syndrome (prevalence ratio 1.57, 95% CI 1.25-1.98). The findings suggest that CS(2) poisoning may increase the risk of metabolic syndrome.

Metabolic Syndrome and Mortality in Older Adults

The utility of metabolic syndrome (MetS) for predicting mortality among older adults, the highest-risk population, is not well established. In addition, few studies have compared the predictive utility of MetS to that of its individual risk factors. We evaluated relationships of MetS (as defined by the National Cholesterol Education Program Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults [Adult Treatment Panel III (ATPIII)], International Diabetes Foundation [IDF], and World Health Organization [WHO]) and individual MetS criteria with mortality between 1989 and 2004 among 4258 US adults 65 years or older and free of prevalent cardiovascular disease (CVD) in the Cardiovascular Health Study, a multicenter, population-based, prospective cohort. Total, CVD, and non-CVD mortality were evaluated. Cox proportional hazards models were used to estimate the mortality hazard ratio (relative risk [RR]) predicted by MetS. At baseline (mean age, 73 years), 31% of men and 38% of women had MetS (ATPIII). During 15 years of follow-up, 2116 deaths occurred. After multivariable adjustment, compared with persons without MetS, those with MetS had a 22% higher mortality (RR, 1.22; 95% confidence interval [CI], 1.11-1.34). Higher risk with MetS was confined to persons having elevated fasting glucose level (EFG) (defined as > or = 110 mg/dL [> or = 6.1 mmol/L] or treated diabetes mellitus) (RR, 1.41; 95% CI, 1.27-1.57) or hypertension (RR, 1.26; 95% CI, 1.15-1.39) as one of the criteria; persons having MetS without EFG (RR, 0.97; 95% CI, 0.85-1.11) or MetS without hypertension (RR, 0.92; 95% CI, 0.71-1.19) did not have higher risk. Evaluating MetS criteria individually, we found that only hypertension and EFG predicted higher mortality; persons having both hypertension and EFG had 82% higher mortality (RR, 1.82; 95% CI, 1.58-109). Substantially higher proportions of deaths were attributable to EFG and hypertension (population attributable risk fraction [PAR%], 22.2%) than to MetS (PAR%, 6.3%). Results were similar when we used WHO or IDF criteria, when we evaluated different cut points of each individual criterion, and when we evaluated CVD mortality. These findings suggest limited utility of MetS for predicting total or CVD mortality in older adults compared with assessment of fasting glucose and blood pressure alone.