Subsequent Development Of Type Research Articles

Antenatal dietary supplementation with myo-inositol for preventing gestational diabetes.

Gestational diabetes with onset or first recognition during pregnancy is an increasing problem worldwide. Myo-inositol, an isomer of inositol, is a naturally occurring sugar commonly found in cereals, corn, legumes and meat. Myo-inositol is one of the intracellular mediators of the insulin signal and correlates with insulin sensitivity in type 2 diabetes. The potential beneficial effect of improving insulin sensitivity suggests that myo-inositol may be useful for women in preventing gestational diabetes. This is an update of a review first published in 2015. To assess if antenatal dietary supplementation with myo-inositol is safe and effective, for the mother and fetus, in preventing gestational diabetes. We searched the Cochrane Pregnancy and Childbirth's Trials Register, ClinicalTrials.gov, WHO ICTRP (17 March 2022) and the reference lists of retrieved studies. We included published and unpublished randomised controlled trials (RCTs) including cluster-RCTs and conference abstracts, assessing the effects of myo-inositol for the prevention of gestational diabetes in pregnant women. We included studies that compared any dose of myo-inositol, alone or in a combination preparation, with no treatment, placebo or another intervention. Quasi-randomised and cross-over trials were not eligible. We excluded women with pre-existing type 1 or type 2 diabetes. Two review authors independently assessed studies for inclusion, assessed risk of bias and extracted the data. We checked the data for accuracy. We assessed the certainty of the evidence using the GRADE approach. We included seven RCTs (one conducted in Ireland, six conducted in Italy) reporting on 1319 women who were 10 weeks to 24 weeks pregnant at the start of the studies. The studies had relatively small sample sizes and the overall risk of bias was low. For the primary maternal outcomes, meta-analysis showed that myo-inositol may reduce the incidence of gestational diabetes (risk ratio (RR) 0.53, 95% confidence interval (CI) 0.31 to 0.90; 6 studies, 1140 women) and hypertensive disorders of pregnancy (RR 0.34, 95% CI 0.19 to 0.61; 5 studies, 1052 women). However, the certainty of the evidence was low to very low. For the primary neonatal outcomes, only one study measured the risk of a large-for-gestational-age infant and found myo-inositol was associated with both appreciable benefit and harm (RR 1.40, 95% CI 0.65 to 3.02; 1 study, 234 infants; low-certainty evidence). None of the included studies reported on the other primary neonatal outcomes (perinatal mortality, mortality or morbidity composite). For the secondary maternal outcomes, we are unclear about the effect of myo-inositol on weight gain during pregnancy (mean difference (MD) -0.25 kilogram (kg), 95% CI -1.26 to 0.75 kg; 4 studies, 831 women) and perineal trauma (RR 4.0, 95% CI 0.45 to 35.25; 1 study, 234 women) because the evidence was assessed as being very low-certainty. Further, myo-inositol may result in little to no difference in caesarean section (RR 0.91, 95% CI 0.77 to 1.07; 4 studies, 829 women; low-certainty evidence). None of the included studies reported on the other secondary maternal outcomes (postnatal depression and the development of subsequent type 2 diabetes mellitus). For the secondary neonatal outcomes, meta-analysis showed no neonatal hypoglycaemia (RR 3.07, 95% CI 0.90 to 10.52; 4 studies; 671 infants; very low-certainty evidence). However, myo-inositol may be associated with a reduction in the incidence of preterm birth (RR 0.35, 95% CI 0.17 to 0.70; 4 studies; 829 infants). There were insufficient data for a number of maternal and neonatal secondary outcomes, and no data were reported for any of the long-term childhood or adulthood outcomes, or for health service utilisation outcomes. Evidence from seven studies shows that antenatal dietary supplementation with myo-inositol during pregnancy may reduce the incidence of gestational diabetes, hypertensive disorders of pregnancy and preterm birth. Limited data suggest that supplementation with myo-inositol may not reduce the risk of a large-for-gestational-age infant. The current evidence is based on small studies that were not powered to detect differences in outcomes such as perinatal mortality and serious infant morbidity. Six of the included studies were conducted in Italy and one in Ireland, which raises concerns about the lack of generalisability to other settings. There is evidence of inconsistency among doses of myo-inositol, the timing of administration and study population. As a result, we downgraded the certainty of the evidence for many outcomes to low or very low certainty. Further studies for this promising antenatal intervention for preventing gestational diabetes are encouraged and should include pregnant women of different ethnicities and varying risk factors. Myo-inositol at different doses, frequency and timing of administration, should be compared with placebo, diet and exercise, and pharmacological interventions. Long-term follow-up should be considered and outcomes should include potential harms, including adverse effects.

Studying pediatric health outcomes with electronic health records using Bayesian clustering and trajectory analysis

Use of routinely collected data from electronic health records (EHR) can expedite longitudinal studies that investigate childhood exposures and rare pediatric health outcomes. For instance, characteristics of the body mass index (BMI) trajectory early in life may be associated with subsequent development of type 2 diabetes. Past studies investigating these relationships have used longitudinal cohort data collected over the course of many years to investigate the connection between BMI trajectory and subsequent development of diabetes. In contrast, EHR data from routine clinical care can provide longitudinal information on early-life BMI trajectories as well as subsequent health outcomes without requiring any additional data collection. In this study, we introduce a Bayesian joint phenotyping and BMI trajectory model to address data quality challenges in an EHR-based study of early-life BMI and type 2 diabetes in adolescence. We compared this joint modeling approach to traditional approaches using a computable phenotype for type 2 diabetes or separately estimated BMI trajectories and type 2 diabetes phenotypes. In a sample of 49,062 children derived from the PEDSnet consortium of pediatric healthcare systems, a median 8 (interquartile range [IQR] 5–13) BMI measurements were available to characterize the early-life BMI trajectory. The joint modeling and computable phenotype approaches found that age at adiposity rebound between 5 and 9 years was associated with higher odds of type 2 diabetes in adolescence compared to age at adiposity rebound between 2 and 5 years (joint model odds ratio [OR] = 1.77; computable phenotype OR = 1.88) and that BMI in excess of 140% of the 95th percentile for age and sex at age 9 years was associated with higher odds of type 2 diabetes in adolescence relative to children with BMI from 100 to 120% of the 95th percentile (joint model OR = 6.22; computable phenotype OR = 13.25). Estimates from the separate phenotyping and trajectory model were substantially attenuated towards the null. These results demonstrate that EHR data coupled with modern methodologic approaches can improve efficiency and timeliness of studies of childhood exposures and rare health outcomes.

T45G Adiponectin Gene Polymorphism and its Association with Hyperglycemia in Adult Filipinos Seen at the Philippine General Hospital – A Pilot Study

Introduction. Adiponectin is an adipocytokine known to have anti-inflammatory and anti-atherogenic effects. It appears to impact insulin resistance and the subsequent development of type 2 diabetes mellitus (T2D). The gene encoding adiponectin ADIPOQ, has single nucleotide polymorphisms (SNPs) that can be useful biomarkers to predict development of T2D; with the T/G polymorphism of SNP +45 in exon 2 being the most common.Objective. This study was conducted to evaluate the association of T45G adiponectin gene polymorphism with hyperglycemia among adult Filipinos seen at the outpatient department of the Philippine General Hospital.Methods. This is a matched case-control study, with duration of 12 months. DNA was extracted using the QIAGEN MIDI Blood Extraction Kit. The genomic DNA obtained was then subjected to real time PCR for SNP detection.Results. One hundred (100) adults were enrolled; forty-three (43) had normoglycemia, while fifty seven (57) had hyperglycemia, after a 75-g oral glucose tolerance test. Hyperglycemic subjects were older (44±15.6 years vs. 52±8.3 years, p-value 0.002), and had lower HDL levels (58.5±16.0 mg/dLvs. 47.8+11.8 mg/dL, p-value 0.000). Among thirty-nine (39) participants found to have the T45G adiponectin gene polymorphism, 22 or 56.4% were hyperglycemic while 17 or 43.6% were normoglycemic.Conclusion. There was no significant association observed between the T45G SNP and presence of hyperglycemia.

Probiotic treatment for women with gestational diabetes to improve maternal and infant health and well-being.

Gestational diabetes mellitus (GDM) is carbohydrate intolerance first recognised during pregnancy and associated with complications for mothers and babies. Probiotics are naturally occurring micro-organisms, which when ingested in adequate amounts, may confer health benefits. Evidence of the role of probiotics as treatment for GDM is limited. To evaluate the safety and effectiveness of probiotics in treating women with GDM on maternal and infant outcomes. We searched the Cochrane Pregnancy and Childbirth's Trials Register ClinicalTrials.gov, WHO International Clinical Trials Registry Platform (ICTRP) (24 July 2019), and reference lists of retrieved studies. Randomised controlled trials (RCTs) comparing the use of probiotics versus placebo/standard care for the treatment of GDM. Two review authors independently assessed study eligibility, extracted data, checked data accuracy, and assessed risk of bias of included trials. The certainty of evidence for selected maternal and infant/child outcomes was assessed using GRADE. Nine RCTs (695 pregnant women with GDM) comparing probiotics versus placebo were identified. The overall risk of bias in the nine RCTs was low to unclear and the evidence was downgraded for imprecision due to the small numbers of women participating in the trials. The trials were carried out in hospitals and universities in Iran (seven trials), Thailand (one trial) and Ireland (one trial). All trials compared probiotics with placebo. Maternal outcomes We are uncertain if probiotics have any effect compared with placebo on hypertensive disorders of pregnancy, (risk ratio (RR) 1.50, 95% confidence interval (CI) 0.64 to 3.53; participants = 256; studies = 3; low-certainty evidence) and mode of birth as caesareans (average RR 0.64, 95% CI 0.30 to 1.35; participants = 267; studies = 3; low-certainty evidence) because the certainty of evidence is low and the 95% CIs span possible benefit and possible harm. No trials reported primary outcomes of: mode of birth as vaginal/assisted and subsequent development of type 2 diabetes. We are uncertain if probiotics have any effect compared with placebo on induction of labour (RR 1.33, 95% CI 0.74 to 2.37; participants = 127; studies = 1; very low-certainty evidence). For other secondary maternal outcomes, we are uncertain if there are differences between probiotics and placebo for: postpartum haemorrhage; weight gain during pregnancy intervention and total gestational weight gain; fasting plasma glucose and need for extra pharmacotherapy (insulin). Probiotics may be associated with a slight reduction in triglycerides and total cholesterol. In probiotics compared with placebo, there was evidence of reduction in markers for insulin resistance (HOMA-IR) and HOMA-B; and insulin secretion. There was also an increase in quantitative insulin sensitivity check index (QUICKI). Probiotics were associated with minor benefits in relevant bio-markers with evidence of a reduction in inflammatory markers high-sensitivity C-reactive protein (hs-CRP), interleukin 6 (IL-6), and marker of oxidative stress malondialdehyde; and an increase in antioxidant total glutathione, but we are uncertain if there is any difference in total antioxidant capacity. No trials reported secondary outcomes: perineal trauma, postnatal weight retention or return to pre-pregnancy weight and postnatal depression. Infant/child/adult outcomes We are uncertain if probiotics have any effect, compared with placebo, on the risk of large-for-gestational-age babies (RR 0.73, 95% CI 0.35 to 1.52; participants = 174; studies = 2; low-certainty evidence) or infant hypoglycaemia (RR 0.85, 95% CI 0.39 to 1.84; participants = 177; studies = 3; low-certainty evidence) because the certainty of evidence is low and the 95% CIs span possible benefit and possible harm. No trials reported primary outcomes of: perinatal (fetal/neonatal) mortality; or neurosensory disability. For other secondary outcomes, we are uncertain if there is any difference between probiotics and placebo in gestational age at birth, preterm birth, macrosomia, birthweight, head circumference, length, infant hypoglycaemia, and neonatal intensive care unit (NICU) admissions. There was evidence of a reduction in infant hyperbilirubinaemia with probiotics compared with placebo. No trials reported secondary outcomes: infant adiposity, and later childhood adiposity. There were no adverse events reported by any of the trials. Low-certainty evidence means we are not certain if there is any difference between probiotic and placebo groups in maternal hypertensive disorders of pregnancy, caesareans; and large-for-gestational-age babies. There were no adverse events reported by the trials. Due to the variability of probiotics used and small sample sizes of trials, evidence from this review has limited ability to inform practice. Well-designed adequately-powered trials are needed to identify whether probiotics may improve maternal blood glucose levels and/or infant/child/adult outcomes; and whether they can be used to treat GDM.

P4406New hypothesis of the insulin resistance development: role of adipose-derived stem cell proliferation and adipogenesis

Abstract Background Obesity, remaining a topical issue of modern medicine, leads to development of latent inflammation and insulin resistance in adipose tissue with subsequent development of type 2 diabetes mellitus (T2DM). Among patients with obesity, patients with obesity and normal glucose tolerance (NGT) are often encountered. In our study we have tested the hypothesis that low proliferative potential of adipose derived stromal cells (ADSC) associates with reduced formation of new fat depots, excess accumulation of fat in the functional adipocytes and their hypertrophy, resulting in fat inflammation and insulin resistance. Methods We screened two groups of obese patients with or without T2DM, matched for BMI, age, and duration of obesity to test the hypothesis that hypertrophy and decreased renewal of adipocytes may underlie transition from obesity to T2DM. All patients were matched for carbohydrate metabolism (fasting blood glucose level, glycated hemoglobin, HOMA-IR index and M-index). The subcutaneous and omental fat tissue biopsies were obtained during bariatric surgery from obese individuals with or without T2DM. The morphology and immunophenotype of subcutaneous and omental fat was assessed in frozen tissue sections. ADSC were isolated from both types of fat tissue biopsies and screened for morphology, proliferative potential and inflammatory status. Results The non-diabetic patients had normal carbohydratemetabolism andmoderate insulin resistancemeasured byHOMA-IR and hyperinsulinemic clamp (M-index),while T2DM patientswere extremely insulin resistant by both indexes. The average size of diabetic adipocytes was higher than that of non-diabetic in both subcutaneous and omental fat tissues, indicating adipocyte hypertrophy in T2DM. We have shown that ADSC from T2DM patients had significantly higher level of inflammation. According to measurement of p62 expression and LC3 modification we can say that ADSC from T2DM patients have less autophagy level compare with ADSC from NGT patients. Immunohistochemistry have shown that patients with T2DM have much more infiltration of CD68+-cells in subcutaneous and omental adipose tissue and immunophenotype (balance of M1-M2 macrophages) of adipose tissue at this patients shift toward inflammatory state. Conclusion These results suggest that decreased proliferation and increased hypertrophy of diabetic ADSC may lead to reduced insulin sensitivity via increased inflammation mediated by M1-macrophages and JNK1/2 pathway. Acknowledgement/Funding This work was supported by RSF grant #17-15-01435

Exposure to Gestational Diabetes Mellitus: Impact on the Development of Early-Onset Type 2 Diabetes in Canadian First Nations and Non-First Nations Offspring.

Type 2 diabetes is increasing in children worldwide, with Canadian First Nations (FN) children disproportionally affected. The prevalence of gestational diabetes mellitus (GDM) also is increasing. The objective of this study was to evaluate the impact of GDM exposure in utero and FN status on the subsequent risk of type 2 diabetes in offspring in the first 30 years of life. In this population-based historical prospective cohort study, we used administrative databases linked to a clinical database to explore the independent association and interaction between GDM and FN status on the subsequent development of type 2 diabetes in offspring. Among 321,008 births with a median follow-up of 15.1 years, both maternal GDM and FN status were independently associated with subsequent risk of type 2 diabetes in offspring in the first 30 years of life (hazard ratio 3.03 [95% CI 2.44-3.76; P < 0.0001] vs. 4.86 [95% CI 4.08-5.79; P < 0.0001], respectively). No interaction between GDM and FN status on type 2 diabetes risk was observed. FN status had a stronger impact on the development of type 2 diabetes in offspring than GDM. GDM is an important modifiable risk factor for type 2 diabetes, and its prevention may reduce the prevalence of subsequent type 2 diabetes in offspring. This study adds unique and rigorous evidence to the global public health debate about the impact of GDM on the long-term health of offspring.

Dietary supplementation with myo-inositol in women during pregnancy for treating gestational diabetes.

Dietary supplementation with myo-inositol in women during pregnancy for treating gestational diabetes.

Different intensities of glycaemic control for women with gestational diabetes mellitus.

Gestational diabetes mellitus (GDM) has major short- and long-term implications for both the mother and her baby. GDM is defined as a carbohydrate intolerance resulting in hyperglycaemia or any degree of glucose intolerance with onset or first recognition during pregnancy from 24 weeks' gestation onwards and which resolves following the birth of the baby. Rates for GDM can be as high as 25% depending on the population and diagnostic criteria used and rates are increasing globally. Risk factors associated with GDM include advanced maternal age, obesity, ethnicity, family history of diabetes, and a previous history of GDM, macrosomia or unexplained stillbirth. There is wide variation internationally in glycaemic treatment target recommendations for women with GDM that are based on consensus rather than high-quality trials. To assess the effect of different intensities of glycaemic control in pregnant women with GDM on maternal and infant health outcomes. We searched the Cochrane Pregancy and Childbirth Group's Trials Register (31 January 2016), ClinicalTrials.gov, the WHO International Clinical Trials Registry Platform (ICTRP) (1 February 2016) and reference lists of the retrieved studies. We included one randomised controlled trial. Cluster-randomised and quasi-randomised controlled trials were eligible for inclusion. We used the methods described in the Cochrane Handbook for Systematic Reviews of Interventions for carrying out data collection, assessing study quality and analysing results. Two review authors independently assessed trial eligibility for inclusion, evaluated methodological quality and extracted data for the one included study. We sought additional information from one trial author but had no response. We assessed the quality of evidence for selected outcomes using the GRADE approach. We included one Canadian trial of 180 women, recruited between 20 to 32 weeks' gestation, who had been diagnosed with GDM. Data from 171 of the 180 women were published as a conference abstract and no full report has been identified. The overall risk of bias of the single included study was judged to be unclear.The included trial did not report on any of this review's primary outcomes. For the mother, these were hypertension disorders of pregnancy or subsequent development of type 2 diabetes. For the infant, our primary outcomes were (perinatal (fetal and neonatal) mortality; large-for-gestational age; composite of death or severe morbidity or later childhood neurosensory disability).The trial did report data relating to some of this review's secondary outcomes. There was no clear difference in caesarean section rates for women assigned to using strict glycaemic targets (pre-prandial 5.0 mmol/L (90 mg/L) and at one-hour postprandial 6.7 mmol/L (120 mg/dL)) (28/85, 33%) when compared with women assigned to using liberal glycaemic targets (pre-prandial 5.8 mmol/L (103 mg/dL) and at one-hour postprandial 7.8 mmol/L (140 mg/dL)) (21/86, 24%) (risk ratio (RR) 1.35, 95% confidence interval (CI) 0.83 to 2.18, one trial, 171 women; very low quality). Using the GRADE approach, we found the quality of the evidence to bevery low for caesarean section due to poor reporting of risk of bias, imprecision and publication bias. Strict glycaemic targets were associated with an increase in the use of pharmacological therapy (identified as the use of insulin in this study) (33/85; 39%) compared with liberal glycaemic targets (18/86; 21%) (RR 1.85, 95% CI 1.14 to 3.03; one trial, 171 women). CIs are wide suggesting imprecision and caution is required when interpreting the data. No other secondary maternal outcome data relevant to this review were reported. For the infant, there were no clear differences between the groups of women receiving strict and liberal glycaemic targets for macrosomia (birthweight greater than 4000 g) (RR 1.35, 95% CI 0.31 to 5.85, one trial, 171 babies); small-for-gestational age (RR 1.12, 95% CI 0.48 to 2.63, one trial, 171 babies); birthweight (mean difference (MD) -92.00 g, 95% CI -241.97 to 57.97, one trial, 171 babies) or gestational age (MD -0.30 weeks, 95% CI -0.73 to 0.13, one trial, 171 babies). Adverse effects data were not reported. No other secondary neonatal outcomes relevant to this review were reported. This review is based on a single study (involving 180 women) with an unclear risk of bias. The trial (which was only reported in a conference abstract) did not provide data for any of this review's primary outcomes but did provide data for a limited number of our secondary outcomes. There is insufficient evidence to guide clinical practice for targets for glycaemic control for women with GDM to minimise adverse effects on maternal and fetal health. Glycaemic target recommendations from international professional organisations for maternal glycaemic control vary widely and are reliant on consensus given the lack of high-quality evidence.Further high-quality trials are needed, and these should compare different glycaemic targets for guiding treatment of women with GDM, assess both short-term and long-term health outcomes for women and their babies, include women's experiences and assess health services costs. Four studies are ongoing.

Association between systemic oxidative stress and insulin resistance/sensitivity indices - the PREDIAS study.

Systemic oxidative stress has been causally related to insulin resistance and the subsequent development of type 2 diabetes mellitus (T2D). We investigated associations between circulating oxidative stress markers and different surrogate indexes of insulin sensitivity/resistance. Cross-sectional data were obtained from 1183 subjects with normal glucose tolerance (NGT), 280 subjects with impaired glucose tolerance (IGT) and 69 newly detected T2D individuals entering the PREDIAS (prevention of diabetes) study. Following oral glucose tolerance test, five different insulin sensitivity/resistance indices were estimated: homoeostasis model of insulin resistance (HOMA-IR), quantitative insulin sensitivity check index (QUICKI), early phase insulin release (EPIR), insulin sensitivity index (ISI) and disposition index (DI). Additionally, circulating phagocyte generation of reactive oxygen species (ROS) and plasma total antioxidant capacity (TAC) was measured. After adjustment for five covariates, HOMA-IR was significantly increased in IGT and T2D subjects when compared to NGT subjects (P = 0·000). QUICKI (P = 0·000), ISI (P = 0·000), EPIR (0·005/0·012) and DI (P = 0·000) were significantly attenuated in IGT and T2D. The prevalence of IGT and T2D individuals increased with increasing ROS generation and TAC tertiles. Increased systemic ROS generation was paralleled by increased HOMA-IR (P < 0·001, tertile 1/T1/vs tertile 3/T3/), decreased QUICKI (P < 0·001, T1 vs T3) and decreased ISI (P < 0·05, T1 vs T3). A similar tendency for indices was observed when comparing TAC tertiles: increase in HOMA-IR, decrease in QUICKI and ISI (P < 0·001, T1 vs T3 each). EPIR and DI did not differ significantly across ROS generation and TAC tertiles. Systemic oxidative stress is associated with elevated insulin resistance index HOMA-IR, and decreased insulin sensitivity surrogates QUICKI and ISI.

Long-Term Impact of Gestational Diabetes on Subsequent Development of Type 2 Diabetes in Mothers and Offspring in Manitoba

Long-Term Impact of Gestational Diabetes on Subsequent Development of Type 2 Diabetes in Mothers and Offspring in Manitoba

Reducing the Risk of Developing Diabetes

Reducing the Risk of Developing Diabetes

Abstract P062: Ten Weeks of Daily Consumption of Common Fructose Containing Sugars Does Not Increase Liver Fat Content

Purpose: Evaluate the effect of addition of commonly consumed fructose containing sugars to the usual diet on liver fat content. Background: Fructose induced triglyceride synthesis has been argued to be augmented when accompanied by glucose. As the most common sources of fructose, high fructose corn syrup HFCS) and sucrose, also contain glucose such a response would be particularly detrimental to metabolic health due to the known role of excess fat in the liver in the induction of abnormalities in glucose homeostasis, insulin resistance and the subsequent development of type II diabetes. Methods: For ten weeks, sixty-eight individuals (42.16 ± 11.66 years) consumed low-fat milk sweetened with either HFCS or sucrose such that the added sugar matched the 25th, 50th and 90th percentile population consumption levels of fructose. Fat content of the liver was obtained before and after the ten week intervention. Imaging was performed on a Philips 64-slice CT scanner. Region of interest measurements in the four sectors of the liver delineated by the hepatic veins were obtained in all patients, and converted to hepatocellular fat content percentages. Fat content of the liver remained unchanged (13.32 ±10.49 vs 13.32 ± 10.75%, p &gt; 0.05). Group assignment did not affect the result interaction p &gt; 0.05). Conclusions: These data suggest that ectopic fat storage in the liver is not promoted when fructose is consumed as part of a normal diet, even in amounts as high as the 90th percentile consumption level.

Consumption of sucrose and high-fructose corn syrup does not increase liver fat or ectopic fat deposition in muscles

It has been postulated that fructose-induced triglyceride synthesis is augmented when accompanied by glucose. Chronic elevations could lead to excess fat accumulation in the liver and ectopic fat deposition in muscles, which in turn could contribute to the induction of abnormalities in glucose homeostasis, insulin resistance, and the subsequent development of type 2 diabetes. Our objective was to evaluate the effect of the addition of commonly consumed fructose- and (or) glucose-containing sugars in the usual diet on liver fat content and intramuscular adipose tissue. For 10 weeks, 64 individuals (mean age, 42.16 ± 11.66 years) consumed low-fat milk sweetened with either high-fructose corn syrup (HFCS) or sucrose; the added sugar matched consumption levels of fructose in the 25th, 50th, and 90th percentiles of the population. The fat content of the liver was measured with unenhanced computed tomography imaging, and the fat content of muscle was assessed with magnetic resonance imaging. When the 6 HFCS and sucrose groups were averaged, there was no change over the course of 10 weeks in the fat content of the liver (13.32% ± 10.49% vs. 13.21% ± 10.75%; p > 0.05), vastus lateralis muscle (3.07 ± 0.74 g per 100 mL vs. 3.15 ± 0.84 g per 100 mL; p > 0.05), or gluteus maximus muscle (4.08 ± 1.50 g per 100 mL vs. 4.24 ± 1.42 g per 100 mL; p > 0.05). Group assignment did not affect the result (interaction > 0.05). These data suggest that when fructose is consumed as part of a typical diet in normally consumed sweeteners, such as sucrose or HFCS, ectopic fat storage in the liver or muscles is not promoted.

A prospective observational study of the relationship of critical illness associated hyperglycaemia in medical ICU patients and subsequent development of type 2 diabetes

IntroductionCritical illness is commonly complicated by hyperglycaemia caused by mediators of stress and inflammation. Severity of disease is the main risk factor for development of hyperglycaemia, but not all severely ill develop hyperglycemia and some do even in mild disease. We hypothesised that acute disease only exposes a latent disturbance of glucose metabolism which puts those patients at higher risk for developing diabetes.MethodsMedical patients with no history of impaired glucose metabolism or other endocrine disorder admitted to an intensive care unit between July 1998 and June 2004 were considered for inclusion. Glucose was measured at least two times a day, and patients were divided into the hyperglycaemia group (glucose ≥7.8 mmol/l) and normoglycaemia group. An oral glucose tolerance test was performed within six weeks after discharge to disclose patients with unknown diabetes or pre-diabetes who were excluded. Patients treated with corticosteroids and those terminally ill were also excluded from the follow-up which lasted for a minimum of five years with annual oral glucose tolerance tests.ResultsA five-year follow-up was completed for 398 patients in the normoglycaemia group, of which 14 (3.5%) developed type 2 diabetes. In the hyperglycaemia group 193 patients finished follow-up and 33 (17.1%) developed type 2 diabetes. The relative risk for type 2 diabetes during five years after the acute illness was 5.6 (95% confidence interval (CI) 3.1 to 10.2).ConclusionsPatients with hyperglycaemia during acute illness who are not diagnosed with diabetes before or during the hospitalization should be considered a population at increased risk for developing diabetes. They should, therefore, be followed-up, in order to be timely diagnosed and treated.

Erratum to: A prospective observational study of the relationship of critical illness associated hyperglycaemia in medical ICU patients and subsequent development of type 2 diabetes

Erratum to: A prospective observational study of the relationship of critical illness associated hyperglycaemia in medical ICU patients and subsequent development of type 2 diabetes

Association Between Serum Uric Acid and Development of Type 2 Diabetes

OBJECTIVETo systematically evaluate the association between serum uric acid (SUA) level and subsequent development of type 2 diabetes.RESEARCH DESIGN AND METHODSWe searched Medline (31 March from 1966 to 2009) and Embase (31 March from 1980 to 2009) for observational cohort studies examining the association between SUA and the risk of type 2 diabetes by manual literature search. Relative risks (RRs) for each 1 mg/dl increase in SUA were pooled by using a random-effects model. The studies included were stratified into subgroups representing different study characteristics, and meta-regression analyses were performed to investigate the effect of these characteristics on the association between SUA level and type 2 diabetes risk.RESULTSThe search yielded 11 cohort studies (42,834 participants) that reported 3,305 incident cases of type 2 diabetes during follow-up periods ranging from 2.0 to 13.5 years. The pooled RR of a 1 mg/dl increase in SUA was 1.17 (95% CI 1.09–1.25). Study results were consistently significant (i.e., >1) across characteristics of participants and study design. Publication bias was both visually and statistically suggested (P = 0.03 for Egger's test, 0.06). Adjustment for publication bias attenuated the pooled RR per mg/dl increase in SUA (RR 1.11 [95% CI 1.03–1.20]), but the association remained statistically significant (P = 0.009).CONCLUSIONSThe current meta-analysis suggests that SUA level is positively associated with the development of type 2 diabetes regardless of various study characteristics. Further research should attempt to determine whether it is effective to utilize SUA level as a predictor of type 2 diabetes for its primary prevention.

ACOG Committee Opinion No. 435: Postpartum Screening for Abnormal Glucose Tolerance in Women Who Had Gestational Diabetes Mellitus

Establishing the diagnosis of gestational diabetes mellitus offers an opportunity not only to improve pregnancy outcome, but also to decrease risk factors associated with the subsequent development of type 2 diabetes. The American College of Obstetricians and Gynecologists' Committee on Obstetric Practice recommends that all women with gestational diabetes mellitus be screened at 6-12 weeks postpartum and managed appropriately.

Antibiotic Use and Type 1 Diabetes in Childhood

Indirect evidence is accumulating for an association between antibiotic use, especially in early childhood, and long-term immunologic health. The authors evaluated the association between antibiotic use in childhood and subsequent development of type 1 diabetes. A nationwide cohort study of all Danish singleton children born during 1995-2003 (n = 606,420) was conducted. Incidence rate ratios for type 1 diabetes comparing children according to antibiotic use were estimated. Antibiotic use was classified according to class, number of uses, and age at use. Use of any antibiotic was not associated with type 1 diabetes (rate ratio = 1.16, 95% confidence interval: 0.91, 1.50). Evaluation of type 1 diabetes risk according to number of courses of any antibiotic yielded no association between antibiotic use and type 1 diabetes, with an increase in rate ratio per course of 1.02 (95% confidence interval: 0.97, 1.07). No specific class of antibiotics was associated with type 1 diabetes, no specific age of use was associated with type 1 diabetes, and no specific age at onset of type 1 diabetes was associated with antibiotics. In a large nationwide prospective study, no association between antibiotic use and type 1 diabetes was found among Danish children.

Pediatric metabolic syndrome: A growing threat

The prevalence of the metabolic syndrome (MS) is high among obese children and adolescents and increases with the severity of the obesity, and with central adiposity in particular. In addition, adverse biochemical markers of cardiovascular risk are already present in this population. The metabolic syndrome is an important risk factor for subsequent development of type 2 diabetes and/or cardiovascular diseases. Therefore, the key clinical implication of a diagnosis of MS is identification of a patient needing aggressive lifestyle modification focused on weight reduction and increased physical activity. In contrast to the data from adults, long-term cardiovascular risk in children and adolescents with the MS has not been clearly determined.

Breast-feeding and diabetes: Long-term impact on mothers and their infants

In the general population, breast-feeding is associated with a reduced risk of the offspring being overweight later in life by 22% to 24% across the age spectrum, from preschool children to adults. There is a dose-response gradient with increasing duration of breast-feeding, and lowest risk with prolonged, exclusive breast-feeding. Breast-feeding has been shown to slow infant growth up to 2 years of age. By contrast, the scientific evidence is inconclusive about whether breast-feeding protects against the onset of overweight and subsequent development of type 2 diabetes among offspring whose mothers had diabetes during pregnancy. Moreover, evidence is insufficient to determine if lactation protects against development of type 2 diabetes later in life in women with a diabetes history during pregnancy. Given the paucity of the evidence and equivocal findings about the long-term effects of breast-feeding on future health of women with diabetes during pregnancy and their infants, further research is recommended.