Development Of Impaired Fasting Glucose Research Articles

Sarcopenia and Appendicular Muscle Mass as Predictors of Impaired Fasting Glucose/Type 2 Diabetes in Elderly Women.

Elderly women exhibit a high risk of type 2 diabetes (T2D), but no definitive data exist about the possible role of postmenopausal increases in visceral adiposity, the loss of lean body mass, or decreases in the sum of the lean mass of arms and legs (appendicular skeletal muscle mass (ASMM)). This retrospective, longitudinal study investigated whether body composition (bioelectrical impedance analysis) predicted the development of impaired fasting glucose (IFG) or T2D in a cohort of 159 elderly women (age: 71 ± 5 years, follow-up: 94 months) from southern Italy (Clinical Nutrition and Geriatric Units of the “Mater Domini” University Hospital in Catanzaro, Calabria region, and the “P. Giaccone ”University Hospital in Palermo, Sicily region). Sarcopenia was defined in a subgroup of 128 women according to the EWGSOP criteria as the presence of low muscle strength (handgrip strength <16 kg) plus low muscle mass (reported as appendicular skeletal muscle mass <15 kg). Participants with a low ASMM had a higher IFG/T2D incidence than those with a normal ASMM (17% vs. 6%, p-adjusted = 0.044); this finding was independent of BMI, fat mass, waist circumference, and habitual fat intake (OR = 3.81, p = 0.034). A higher incidence of IFG/T2D was observed in the subgroup with sarcopenia than those without sarcopenia (33% vs. 7%, p-adjusted = 0.005) independent of BMI and fat mass (OR = 6.75, p = 0.007). In conclusion, this study demonstrates that elderly women with low ASMM had a higher probability of developing IFG/T2D. Further studies are needed to confirm these results in men and in other age groups.

Nonalcoholic fatty liver disease is a risk factor for glucose intolerance onset in men regardless of alanine aminotransferase status.

IntroductionFatty liver disease (FLD) is a surrogate condition for glucose intolerance development. FLD may involve normal or abnormal liver enzyme levels. Whether FLD is a risk factor for glucose intolerance, regardless of liver enzyme levels, remains unknown. We assessed relationships between the development of impaired fasting glucose (IFG) and FLD, liver enzyme abnormalities, and alcohol consumption.Materials and MethodsWe retrospectively evaluated 8,664 participants with more than two annual health check‐ups. Participants were classified according to sex, alcohol consumption, alanine aminotransferase (ALT) levels, and fatty liver status.ResultsIn univariate analyses, IFG onset among men was related to normal or high ALT levels with FLD in the nonalcoholic and alcoholic groups (P‐trend < 0.01). In multivariate analyses, IFG onset among nonalcoholic men was associated with normal or high ALT levels with FLD, independent of potential confounding factors (P‐trend < 0.01). However, IFG onset was non‐independently associated with any condition among alcoholic men. In univariate analyses, IFG onset among women was related to normal or high ALT levels with FLD in the nonalcoholic group (P‐trend < 0.01) and high ALT levels with FLD in the alcoholic group (P‐trend < 0.05). In multivariate analyses, IFG onset was independently associated with only normal ALT levels in nonalcoholic FLD women.ConclusionsAmong nonalcoholic men and women, FLD was a risk factor for IFG onset, including normal ALT concentrations. Care is needed for individuals with nonalcoholic FLD, regardless of liver injury, possibly helping reduce glucose intolerance risk.

Effect of Cigarette Smoking on Fasting Serum Glucose in Healthy Male Population

Acute effects of cigarette smoking include impaired insulin action that leads to abnormal glucose metabolism. Smoking is an independent risk factor for type 2 diabetes which is one of the global health crises and insulin resistance is one of the main risk factors for cardiovascular disease. This cross-sectional study was done to examine whether fasting serum glucose differs between cigarette smokers compared to non-smokers and to investigate the association of cigarette smoking with the development of impaired fasting glucose and type 2 diabetes. This study was done in the Physiology department of Mymensingh Medical College, an outpatient department of Mymensingh Medical College Hospital, for over a period of one year from July 2014 to June 2015. Fasting serum blood glucose was done by enzymetric colorometric GOD-PAP method in a total of 150 subjects, in which non-smokers were 50 and numbers of smokers were 100 with the duration of smoking 5 - 10 years and &gt;10 years. A questionnaire including data was completed in all cases. The data were checked, coded, and entered into an SPSS 11.5. Statistical significance of difference among the groups was calculated by Students unpaired t' test. P-value &lt;0.05 was considered as a level of significance. Fasting Serum Glucose level was increased gradually with the duration of smoking in smokers than the non-smokers. Results were statistically highly significant. Fasting Serum Glucose gradually increase with the duration of smoking and results were within the physiological limit in two study groups (Group-II A with 5-10 years duration of smoking and Group- II B with more than 10 years duration of smoking) but not statistically significant. This study showed cigarette smoking has deleterious effects on insulin metabolism causing an increase in serum glucose with duration of smoking period.&#x0D; CBMJ 2019 July: Vol. 08 No. 02 P: 36-39

Follow-up at 1\xa0year and beyond of women with gestational diabetes treated with insulin and/or oral glucose-lowering agents: a core outcome set using a Delphi survey

Aims/hypothesisGestational diabetes mellitus (GDM) is linked with a higher lifetime risk for the development of impaired fasting glucose, impaired glucose tolerance, type 2 diabetes, the metabolic syndrome, cardiovascular disease, postpartum depression and tumours. Despite this, there is no consistency in the long-term follow-up of women with a previous diagnosis of GDM. Further, the outcomes selected and reported in the research involving this population are heterogeneous and lack standardisation. This amplifies the risk of reporting bias and diminishes the likelihood of significant comparisons between studies. The aim of this study is to develop a core outcome set (COS) for RCTs and other studies evaluating the long-term follow-up at 1 year and beyond of women with previous GDM treated with insulin and/oral glucose-lowering agents.MethodsThe study consisted of three work packages: (1) a systematic review of the outcomes reported in previous RCTs of the follow-up at 1 year and beyond of women with GDM treated with insulin and/or oral glucose-lowering agents; (2) a three-round online Delphi survey with key stakeholders to prioritise these outcomes; and (3) a consensus meeting where the final COS was decided.ResultsOf 3344 abstracts identified and evaluated, 62 papers were retrieved and 25/62 papers were included in this review. A total of 121 outcomes were identified and included in the Delphi survey. Delphi round 1 was emailed to 835 participants and 288 (34.5%) responded. In round 2, 190 of 288 (65.9%) participants responded and in round 3, 165 of 190 (86.8%) participants responded. In total, nine outcomes were selected and agreed for inclusion in the final COS: assessment of glycaemic status; diagnosis of type 2 diabetes since the index pregnancy; number of pregnancies since the index pregnancy; number of pregnancies with a diagnosis of GDM since the index pregnancy; diagnosis of prediabetes since the index pregnancy; BMI; post-pregnancy weight retention; resting blood pressure; and breastfeeding.Conclusions/interpretationThis study identified a COS that will help bring consistency and uniformity to outcome selection and reporting in clinical trials and other studies involving the follow-up at 1 year and beyond of women diagnosed with GDM treated with insulin and/or oral glucose-lowering agents during pregnancy.

Is a Diabetes Mellitus–Linked Amino Acid Signature Associated With β-Blocker–Induced Impaired Fasting Glucose?

Background— The 5-amino acid (AA) signature, including isoleucine, leucine, valine, tyrosine, and phenylalanine, has been associated with incident diabetes mellitus and insulin resistance. We investigated whether this same AA signature, single-nucleotide polymorphisms in genes in their catabolic pathway, was associated with development of impaired fasting glucose (IFG) after atenolol treatment. Methods and Results— Among 234 European American participants enrolled in the Pharmacogenomic Evaluation of Antihypertensive Responses (PEAR) study and treated with atenolol for 9 weeks, we prospectively followed a nested cohort that had both metabolomics profiling and genotype data available for the development of IFG. We assessed the association between baseline circulating levels of isoleucine, leucine, valine, tyrosine, and phenylalanine, as well as single-nucleotide polymorphisms in branched-chain amino-acid transaminase 1 (BCAT1) and phenylalanine hydroxylase (PAH ) with development of IFG. All baseline AA levels were strongly associated with IFG development. Each increment in standard deviation of the 5 AAs was associated with the following odds ratio and 95% confidence interval for IFG based on a fully adjusted model: isoleucine 2.29 (1.31–4.01), leucine 1.80 (1.10–2.96), valine 1.77 (1.07–2.92), tyrosine 2.13 (1.20–3.78), and phenylalanine 2.04 (1.16–3.59). The composite P value was 2×10 −5 . Those with PAH (rs2245360) AA genotype had the highest incidence of IFG ( P for trend=0.0003). Conclusions— Our data provide important insight into the metabolic and genetic mechanisms underlying atenolol-associated adverse metabolic effects. Clinical Trial Registration— http://www.clinicaltrials.gov ; Unique Identifier: NCT00246519

New Onset Diabetes and Impaired Fasting Glucose After Liver Transplant: Risk Analysis and the Impact of Tacrolimus Dose

New onset diabetes mellitus after transplant is one of the major metabolic complications after liver transplant. Development of impaired fasting glucose after liver transplant is thought to be associated with increased risk of cardiovascular mortality and has not been well studied before. The aim of this study was to evaluate incidence and risk factors of new onset diabetes mellitus after transplant and impaired fasting glucose in liver transplant patients. In a cross-sectional study, all adult patients (aged≥18 years) who were transplanted because of chronic liver diseases from June 2002 to September 2010 at Shiraz Liver Transplant Center were evaluated for developing diabetes and impaired fasting glucose. Totally, 86 patients (18.81%) were found to have diabetes after liver transplant. Forty patients (27 men and 13 women; 8.75%) developed new onset diabetes mellitus after transplant and 36 patients (7.87%) developed impaired fasting glucose after liver transplant. The mean age of patients with new onset diabetes mellitus after transplant was higher than that of nondiabetic patients (P = .001). Mean fasting plasma glucose before liver transplant was significantly higher in diabetic patients compared with nondiabetic patients (P = .002) (5.20±0.93 mmol/L vs 4.44±0.56 mmol/L) (93.86±16.80 mg/dL vs 80±10.14 mg/dL). Patients with new onset diabetes mellitus after transplant received higher doses of tacrolimus as immunosuppressive medication than nondiabetic patients (P = .001). Fasting plasma glucose before transplant can predict development of new onset diabetes mellitus after transplant. Age and tacrolimus dosage are independent risk factors for new onset diabetes mellitus after transplant in our patients.

Association of amylin in the development of impaired fasting glucose and impaired glucose tolerance

Objective: The present study was planned to explore the role of amylin in the pathogenesis of impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) subjects. Subjects and Methods: In this study, 20 IFG and 25 IGT subjects along with 30 healthy subjects were included. Plasma glucose (fasting and 2 h after 75 g glucose) was measured by glucose oxidase method, serum triglyceride and total cholesterol, high density lipoprotein (HDL) and low density lipoprotein (LDL) by enzymatic method. Serum insulin and amylin were measured by the enzyme-linked immunosorbent assay method. B-cell secretory capacity (Homeostasis model assessment [HOMA] %B) and insulin sensitivity (HOMA %S) were estimated by HOMA-CIGMA software. Results: Age and body mass index were matched among control and the hyperglycemic groups (IFG, IGT). Fasting total cholesterol, HDL and LDL was significantly higher in IGT subjects compared with control and IFG subjects. Plasma insulin was significantly higher in IFG and IGT compared with control subjects (median [range], pmol/l; control, 38 [28-55]; IFG, 49 [40-56] and IGT, 60 [20-91]). HOMA %B was significantly lower in IFG and significantly higher in IGT subjects compared with the controls (median [range], %; control, 81 [53-156]; IFG, 52 [40-63] and IGT, 95 [33-195]). HOMA %S was significantly decreased in IGT and also in IFG compared to controls (median (range), %; control, 137 [95-187]; IFG, 104 [88-127] and IGT, 86 [57-255]). Plasma amylin was significantly raised in IFG and IGT compared to control subjects (mean ± standard deviation, pmol/l; control, 5.0 ± 0.63; IFG, 6.43 ± 0.67 and IGT, 8.0 ± 1.18). In binary logistic regression analysis, it has been found that plasma amylin concentration is positively associated with impaired glucose regulation and in bivariate correlation analysis it has been found that plasma amylin is positively associated with HOMA %B and negatively associated with fasting glucose. Conclusion: The present data suggested that increased amylin concentration may be contributed to the development of pre-diabetic condition or vice versa.

Insulin resistance with impaired fasting glucose increases the risk of NAFLD

Background: Our aim was to investigate the frequency of elevated liver enzymes and NAFLD in patients with known insulin resistance during 15 years of follow-up. Methods: Subjects with insulin resistance were identified from a population-based prospective cohort study in Sweden, Malm? Diet and Cancer Study, conducted in 1991-1996. Inall, 285 non-diabetic subjects with insulin resistance established by HOMA-IR (homeostasis model assessment) were invited to do the liver function testing and if elevated, they should be further assessed by radiological examination of the liver, anthropometric measures and blood testing. Results: 165 subjects (57.9%) agreed to do the liver function testing. Of these, 25 subjects (15%) had elevated liver enzymes. After exclusion of other diseases, 5 of the remaining 21 subjects (23.8%) had radiological signs of steatosis. Liver steatosis significantly correlated with ALT (alanine aminotransferase) (p = 0.04), HOMA-IR (p = 0.00) and the metabolic syndrome (p = 0.03). 80% of the subjects with NAFLD had either developed type 2 diabetes mellitus or had impaired fasting glucose and 80% fulfilled the WHO-criteria for the metabolic syndrome, which were of significant differences to the group without NAFLD. Conclusion: The risk of developing elevated liver enzymes and NAFLD at long-term follow-up in insulin resistant subjects is not insignificant, but mainly associated with the simultaneous development of impaired fasting glucose, established diabetes mellitus and/ or the metabolic syndrome.

Elevated Properdin and Enhanced Complement Activation in First-Degree Relatives of South Asian Subjects With Type 2 Diabetes

OBJECTIVEEmerging data implicate activation of the complement cascade in the pathogenesis of type 2 diabetes. The objective of the current study was to evaluate the relationships between components of the complement system, metabolic risk factors, and family history of type 2 diabetes in healthy South Asians.RESEARCH DESIGN AND METHODSWe recruited 119 healthy, first-degree relatives of South Asian subjects with type 2 diabetes (SARs) and 119 age- and sex-matched, healthy South Asian control subjects (SACs). Fasting blood samples were taken for measurement of complement factors and standard metabolic risk factors.RESULTSSARs were characterized by significantly higher properdin (mean concentration 12.6 [95% CI 12.2–13.1] mg/L vs. SACs 10.1 [9.7–10.5] mg/L, P < 0.0001), factor B (187.4 [180.1–195.0] mg/L vs. SACs 165.0 [158.0–172.2] mg/L, P < 0.0001), and SC5b-9 (92.0 [86.1–98.3] ng/mL vs. SACs 75.3 [71.9–78.9] ng/mL, P < 0.0001) and increased homeostasis model assessment of insulin resistance (2.86 [2.61–3.13] vs. SACs 2.31 [2.05–2.61], P = 0.007). C-reactive protein did not differ between SARs and SACs (P = 0.17). In subgroup analysis of 25 SARs and 25 SACs with normal oral glucose tolerance tests, properdin, factor B, and SC5b-9 remained significantly elevated in SARs.CONCLUSIONSIncreased properdin and complement activation are associated with a family history of type 2 diabetes in South Asians independent of insulin resistance, and predate the development of impaired fasting glucose and impaired glucose tolerance. Properdin and SC5b-9 may be novel biomarkers for future risk of type 2 diabetes in this high-risk population and warrant further investigation.

Objectively Measured Physical Activity and the Subsequent Risk of Incident Dysglycemia

OBJECTIVETo investigate pedometer-measured physical activity (PA) in 2000 and change in PA over 5 years with subsequent risk of dysglycemia by 2005.RESEARCH DESIGN AND METHODSThis prospective cohort study in Tasmania, Australia, analyzed 458 adults with normal glucose tolerance and a mean (SD) age of 49.7 (12.1) years in 2000. Variables assessed in 2000 and 2005 included PA, by pedometer and questionnaire, nutrient intake, and other lifestyle factors. Incident dysglycemia was defined as the development of impaired fasting glucose or impaired glucose tolerance revealed by oral glucose tolerance testing in 2005, without type 2 diabetes.RESULTSIncident dysglycemia developed in 26 participants during the 5-year period. Higher daily steps in 2000 were independently associated with a lower 5-year risk of incident dysglycemia (adjusted odds ratio [AOR] 0.87 [95% CI 0.77–0.97] per 1,000-step increment). Higher daily steps in 2005, after controlling for baseline steps in 2000 (thus reflecting change in steps over 5 years), were not associated with incident dysglycemia (AOR 1.02 [0.92–1.14]). Higher daily steps in 2000 were also associated with lower fasting blood glucose, but not 2-h plasma glucose by 2005. Further adjustment for BMI or waist circumference did not remove these associations.CONCLUSIONSAmong community-dwelling adults, a higher rate of daily steps is associated with a reduced risk of incident dysglycemia. This effect appears to be not fully mediated through reduced adiposity.

Short Sleep Duration is Associated with the Development of Impaired Fasting Glucose: The Western New York Health Study

To examine whether sleep duration was associated with incident-impaired fasting glucose (IFG) over 6 years of follow-up in the Western New York Health Study. Participants (N = 1,455, 68% response rate) who were free of type 2 diabetes and known cardiovascular disease at baseline (1996-2001) were reexamined in the period 2003-2004. A nested case-control study was conducted. Cases had fasting plasma glucose (FPG) less than 100 mg/dL at baseline and 100 to 125 mg/dL at follow-up: controls (n = 272) had FPG less than 100 mg/dL at both exams. Cases (n = 91) were individually matched to three controls (n = 272) on sex, race, and year of study enrollment. Average sleep duration was categorized as short (<6 hours), mid-range (6 to 8 hours), and long (>8 hours). In multivariate conditional logistic regression after adjustment for several diabetes risk factors, the odds ratio (OR) of IFG among short sleepers was 3.0 (95% confidence limit [CL]: 1.05, 8.59) compared to mid-range sleepers. There was no association between long sleep and IFG: OR 1.6 (95% CL: 0.45, 5.42). Adjustment for insulin resistance attenuated the association only among short sleepers: OR 2.5 (95% CL: 0.83, 7.46). Short sleep duration was associated with an elevated risk of IFG. Insulin resistance appears to mediate this association.

Hyperinsulinemia and metabolic syndrome at mean age of 10 years in black and white schoolgirls and development of impaired fasting glucose and type 2 diabetes mellitus by mean age of 24 years

The objective of the study was to evaluate preteen insulin and metabolic syndrome (MS) as independent predictors of impaired fasting glucose (IFG) and type 2 diabetes mellitus (T2DM) in black and white females by mean age of 24 years. This was a prospective cohort study. There were 8 measures of fasting glucose and insulin from mean age of 10 years through mean age of 24 years, and insulin also at mean age of 25 years. Childhood MS was defined by at least 3 abnormal values among waist circumference, triglyceride, high-density lipoprotein cholesterol, blood pressure, and glucose. Hyperinsulinemia was defined by insulin greater than or equal to race-specific 75th percentile. Patients with type 1 diabetes mellitus were excluded. The study was held in schools and in an outpatient clinical center. Participants were schoolgirls (260 white, 296 black). There was no intervention. The outcome measures were IFG (fasting glucose of at least 100 to 125 mg/dL) and T2DM (fasting glucose of at least 126 mg/dL). By the age of 24 years, there were 11 cases of T2DM (2%) and 108 cases of IFG (19%). By the age of 24 years, IFG + T2DM was present in 18% of women (73/412) who had normal insulin–no MS at the age of 10 years vs 28% (34/122) of those with high insulin–no MS at the age of 10 years (P = .014) and 67% (10/15) of those with high insulin + MS at the age of 10 years (P < .0001). By stepwise logistic regression, significant, independent, positive predictors of IFG + T2DM were first insulin measure in childhood, age at last sampling, childhood MS, change in body mass index over 15 years, and, separately, initial glucose of at least 100 mg/dL and average of all insulin quartile ranks over 15 years. The correlation between childhood insulin z score and insulin z score 15 years later was r = .30, P < .0001. Insulin and MS at a mean age of 10 years plus change in body mass index over 15 years, and 15-year average insulin rank independently predict IFG + T2DM by mean age of 24 years, suggesting avenues for primary prevention.

Early Insulin Secretory Dysfunction in Korean Prediabetic Subjects: Should We Change the Criteria for "Prediabetes?"

Early Insulin Secretory Dysfunction in Korean Prediabetic Subjects: Should We Change the Criteria for "Prediabetes?"

Alcohol consumption and higher incidence of impaired fasting glucose or type 2 diabetes in obese Korean men

It is inconclusive whether moderate alcohol consumption reduces the diabetes risk. We observed the development of impaired fasting glucose or type 2 diabetes according to the amount of alcohol intake and body mass index. The annual health evaluation data of 2,500 male workers from 2002 to 2006 were reviewed retrospectively deleting personal identification code. The information contained sex, age, medical history, smoking status, alcohol consumption, participating regular exercise, anthropometric, and biochemistry measurement. Impaired fasting glucose or diabetes was determined when fasting plasma glucose was ≥100 mg/dL. Thousand seven hundred seven subjects were eligible after excluding medical history of diabetes or fasting glucose ≥100 mg/dL at baseline. The relative risks of its development in group of taking 1–14, 15–29, and ≥30.0 g ethanol were 0.842 (95% confidence interval [CI], 0.603–1.176), 1.068 (95% CI, 0.736–1.551), and 1.019 (95% CI, 0.662–1.568) within normal weight group, 1.164 (95% CI, 0.795–1.705), 1.421 (95% CI, 0.947–2.133), and 1.604 (95% CI, 1.031–2.495) within overweight group, and 1.498 (95% CI, 1.042–2.153), 1.634 (95% CI, 1.091–2.447), and 1.563 (95% CI, 1.019–2.396) within obese group each after adjusting age, family history of diabetes, smoking, exercise, serum fasting glucose, aspartate aminotransferase, and γ-glutamyltransferase with nondrinkers as a reference group. Not only high alcohol consumption but also moderate drinking was related with higher incidence of impaired fasting glucose or diabetes in obese Korean men.

Prevalence of diabetes mellitus in the rural southern Free State

SA Fam Pract 2009;51(6):502-505 Background: A worldwide increase in the prevalence of diabetes mellitus (DM) has been reported and an even further increase is expected as a result of lifestyle changes. The objectives of this study were to determine the prevalence of DM in the rural southern Free State and to investigate the contribution of risk factors such as age, physical activity, body mass index (BMI), waist-to-hip ratio and waist circumference to the development of impaired fasting glucose (IFG) or DM. Methods: Fasting venous plasma glucose (FVPG) levels were obtained from a total of 552 participants from Springfontein (n = 195), Trompsburg (n = 162) and Philippolis (n = 180). Participants were between 25 and 64 years of age, with 28.1% male (mean age 47.3 years) and 71.9% female (mean age 46 years). Anthropometric status was determined using standardised techniques. Levels of physical activity were determined using a 24-hour recall of physical activity as well as frequency of performing certain activities. Relative risks (RR) as well as 95% confidence intervals (95% CI) were used to distinguish significant risk factors for having IFG or DM. Results: In the study population the prevalence of DM was 7.6% (5.2% in men and 8.6% in women) and that of IFG was 6.3% (4.5% in men and 7.1% in women). The majority of nondiabetic (34%), IFG (55%) and DM (61%) participants were between the ages of 51 and 60 years. Age was found to be a statistically significant risk factor for having IFG or DM in participants older than 40 years of age (RR 2.3; 95% CI (1.22; 4.34)). Crude measurements (not age- and gender-adjusted) of waist circumference (RR 3.23; 95% CI (1.82; 5.74)), BMI (RR 2.32; 95% CI (1.43; 3.78)) and waist-to-hip ratio (RR 2.51; 95% CI (1.55; 4.07)) were statistically significant risk factors for having IFG or DM. Physical inactivity in men ≥ 40 years was also a statistically significant risk factor (RR 3.23; 95% CI (1.15; 9.05)) for having IFG or DM. Conclusions: In this study, 37.5% of diabetics were newly discovered. A high waist circumference, BMI and waist-to-hip-ratio were associated with an increased risk for developing IFG or DM, with a high waist circumference being the most significant general risk factor. Physically inactive men (≥ 40 years) were also at a higher risk of having IFG or DM. Follow-up FVPG and glucose tolerance tests should be performed on participants in the IFG group. A need for intervention regarding the identification and treatment of DM in these rural areas has been identified. a van Wyk HJ, MBChB, MMed (Clin Pathol) b

Comparison of indices of insulin resistance with metabolic syndrome classifications to predict the development of impaired fasting glucose in overweight and obese subjects: a 3-year prospective study

To compare the ability of biochemical indices of insulin resistance (IR) with metabolic syndrome (MetS) classifications to predict changes in blood glucose control over a 3-year period in overweight and obese subjects. This was a longitudinal, prospective study, with data collected at baseline, 18 and 36 months. A total of 175 overweight (body mass index (BMI)>25 kg m(-2)) and obese (BMI>30 kg m(-2)) subjects were enrolled in the study. The IR indices assessed included fasting insulin concentration, the insulin/glucose-derived indices, homeostasis assessment model of insulin resistance (HOMA-IR) and quantitative insulin sensitivity check index (QUICKI), the insulin/triglyceride-derived McAuley index, plasma adiponectin concentration and the triglyceride (trig) and high-density lipoprotein (HDL)-cholesterol ratio (trig:HDL). The two MetS classifications were assessed according to the definitions of the National Cholesterol Education Program-Third Adult Treatment Panel (NCEP-ATPIII) and the International Diabetes Federation (IDF). The potential of the IR indices and MetS classifications at baseline to predict the development of impaired fasting glucose (IFG) was examined using receiver-operator characteristic (ROC) curve analysis and analysis of variance. Complete data were collected on 158 subjects. In all, 51 (32%) subjects developed IFG during the study. The analysis of variance showed significant differences between the IFG and normoglycaemic group in the baseline values of the McAuley index, trig:HDL, plasma adiponectin concentration and prevalence of the MetS. The ROC curve analysis confirmed this result and showed that the strongest predictors of IFG were baseline trig:HDL and IDF MetS classification, followed in order by the McAuley index, plasma adiponectin concentration and NCEP-ATPIII MetS classification. In contrast, the baseline values of fasting insulin, HOMA-IR and QUICKI did not predict IFG. This study showed that the IR indices, derived, in part, from plasma triglyceride concentration, were sensitive predictors for the development of IFG in normoglycaemic overweight and obese subjects. Indices derived from glucose and insulin did not identify this at-risk group. The study also showed that the presence of MetS and its abnormalities of an increased trig:HDL ratio and low plasma adiponectin concentration were all sensitive predictors of IFG.

Severity of liver disease predicts the development of glucose abnormalities in patients with chronic hepatitis B or C following achievement of sustained virological response to antiviral therapy

A higher prevalence of glucose abnormalities has been reported in patients with hepatitis C virus (HCV) infection compared to patients with hepatitis B virus (HBV) infection. However, previous studies considered some confounding factors and ignored others, which might influence the comparative risk assessment between HBV and HCV infections. Fasting plasma glucose concentration, severity of liver disease and viral load were determined in 220 patients with HCV genotype 4 infection, and 200 patients with HBV infection. Patients completing antiviral therapy were followed-up, and the fasting plasma glucose levels were determined in patients with and without sustained virological response. The prevalence of glucose abnormalities in HCV infection (41%) was significantly higher than that in HBV infection (16%). However, when controlling the severity of liver disease and other risk factors, the prevalence of glucose abnormalities in patients with HCV infection was comparable to that in patients with HBV infection. After attaining of sustained virological response, a decrease of the median fasting plasma glucose value was observed only in chronic hepatitis C. In the group of patients with normal fasting plasma glucose levels, an association of nonsustained virological response with the development of impaired fasting glucose was only observed in chronic hepatitis C. The severity of liver disease was a common predictor of impaired fasting glucose in hepatitis B and C infections. These results indicate that high prevalence of glucose abnormalities can be associated with HBV- and HCV-related liver disease, and that clearance of HCV, but not HBV, may improve glucose metabolism.

The Effect of Gamma-Glutamyltransferase on Impaired Fasting Glucose or Type 2 Diabetes in Korean Men

Background: We sought to determine the association between serum gamma-glutamyltransferase (GGT) levels within the normal range and the risk for development of impaired fasting glucose (IFG) or type 2 diabetes. Methods: This retrospective cohort study spanned four years (2002~2006) with 1,717 Korean men who underwent periodic health examinations at a university hospital in Incheon, Korea and were not diagnosed with IFG or type 2 diabetes. Fasting plasma glucose levels were measured at the annual health examination. IFG and diabetes were defined as a serum fasting glucose concentration of 100~125 mg/dL and more than 126 mg/dL, respectively. Cox's proportional hazards model was used to evaluate the association between serum GGT levels and development of IFG or type 2 diabetes. Results: There was a strong dose-response relationship between serum GG T levels and the incidence of IFG and diabetes. A total of 570 cases (33.2%) of incident IFG and 50 cases (2.9%) of diabetes were found. After controlling potential predictors, the relative risks for the incidence of IFG for GGT levels ≤ 19, 20~25, 26~34, 35~50 and ≥ 51 were 1.00, 0.99, 1.17, 1.23 and 1.38 respectively (P for trend 0.015), and for the incidence of diabetes were 1.00, 1.44, 1.80, 2.55 and 2.58 respectively (P for trend 0.050). Conclusion: The risk for development of IFG and type 2 diabetes increased in a dose-dependent manner as serum GGT increased within its normal range in Korean men. (Korean Diabetes J 33:215-224, 2009)

Pre-teen insulin resistance predicts weight gain, impaired fasting glucose, and type 2 diabetes at age 18–19 y: a 10-y prospective study of black and white girls

BackgroundIdentifying early pre-teen predictors of adolescent weight gain and the development of impaired fasting glucose (IFG) and type 2 diabetes (T2DM) at age 18–19 y could provide avenues for prevention. ObjectiveWe evaluated possible pre-teen predictors for development of IFG, T2DM, and changes in body mass index at age 18–19 y in black and white girls. DesignIn a prospective cohort study, body habitus and fasting insulin and glucose were measured at ages 9–10 and 18–19 y, and multiple 3-d diet records were collected. Factors predicting 10-y change in body mass index and development of IFG and T2DM together were assessed. ResultsIn multivariate analyses, 10-y change in homeostatic model assessment of insulin resistance (HOMA-IR) and the age 9–10 y HOMA-IR × percentage of calories from fat interaction were positive predictors of 10-y changes in body mass index. At age 18–19 y, there were 5 incident cases of T2DM, 37 cases of IFG, and 597 noncases. Age 9–10 y IFG and HOMA-IR (or insulin), 10-y change in HOMA-IR (or insulin), and the age 9–10 y insulin × total caloric intake interaction predicted IFG and T2DM at age 18–19 y. ConclusionsPre-teen IFG, insulin resistance (and insulin), and rapidly increasing insulin resistance during adolescence identifies girls who are at greater risk of future IFG and T2DM. In addition, insulin resistance, interacting with high-fat diets, identifies girls who are at risk of greater weight gain. These findings could open avenues to primary prevention of obesity, IFG, and T2DM in children.

Long‐term changes and variability in diabetes risk factors prior to the development of impaired glucose homeostasis

To determine whether rate of change and variability in risk factors provides insight into the development of impaired fasting glucose (IFG), impaired glucose tolerance (IGT) or Type 2 diabetes (DM). In a nested case-control study, repeated risk factor measurements (mean number 4.3, duration 11.4 years) culminated in 59 men developing IFG (n = 37), IGT (n = 14) and/or DM (n = 11). For each case, two control subjects were matched for age and equivalence of follow-up. Rates of change and variability in diabetes risk factors prior to diagnosis were quantified by regression analysis. Changes between penultimate and diagnostic visits were also analysed. The age-related rise in body mass index (BMI) was attenuated prior to IFG compared with control subjects (+0.102 vs. +0.772 kg/m2/decade, P = 0.02). There was also some evidence for this prior to IGT and DM (IGT: -1.530 vs. +0.158 kg/m2/decade, P = 0.09; DM: -1.146 vs. +0.332 kg/m2/decade, non-significant). Prior to onset, IGT cases were distinguished by higher inflammatory marker levels, a decline in insulinogenic index and greater variability in oral glucose tolerance test (OGTT) insulin, and DM cases by lower insulin sensitivity and higher liver enzyme activities. Fasting and OGTT glucose levels changed little during the mean 8.9 years prior to onset of IFG, IGT or DM. The transition to IGT or DM was accompanied by a fall in insulin sensitivity. Except for BMI, change or variability in risk factor levels appears relatively unimportant in the development of clinically elevated glucose levels. Deterioration in glucose levels to IGT or DM occurs as a rapid, incremental increase accompanied by a decline in insulin sensitivity.