Aim: To investigate the pathophysiological role of different biomarkers in diabetic kidney disease (DKD) among normoalbuminuric patients with a low-estimated glomerular filtration rate (eGFR). Meth...

Diabetes is a chronic condition; those with diabetes are at high risk of developing diabetes complications. One important approach to tackle the diabetes burden is to screen for undiagnosed diabetes and to identify factors that lead to the risk of developing diabetes in the future. The earlier identification of individuals at risk of developing diabetes is crucial for delaying or preventing the onset of type 2 diabetes. Numerous studies have demonstrated that circulating concentrations of branch chain amino acids (BCAAs) predict the risk for developing diabetes; thus, contributing to the recent resurgence of interest in these common analytes. The present review aimed to address the recent findings regarding BCAAs and their role in insulin resistance and diabetes. Recent studies demonstrate that BCAAs are strongly associated with a number of pathological mechanisms causing insulin resistance and type 2 diabetes. The research findings related to BCAA signaling pathways and metabolism broaden our understanding of this topic. However, it remains unclear how increased levels of BCAAs will assist in the prediction of future insulin resistance or type 2 diabetes. Future research needs to determine whether BCAAs are a causative factor for insulin resistance and type 2 diabetes, or just a biomarker of impaired insulin action.

Sex hormone binding globulin (SHBG) is demonstrated to be decreased in subjects with metabolic syndrome (MetS). The aim of the present study was to investigate the association of SHBG in relation to MetS components among men with type 2 diabetes (T2D). This cross-sectional study was carried out among 429 Saudi T2D male patients aged >30 years. Metabolic syndrome was defined using International Diabetes Federation (IDF) criteria. Fasting blood glucose (FBG), HbA1c, albumin, and lipid parameter were measured. Gonadal hormones, namely total testosterone, luteinizing hormone (LH), follicle-stimulating hormone (FSH), and SHBG were determined using ELISA. The SHBG levels of the MetS group was significantly lower than non-MetS group 47.25±31.03 nmol/l vs. 56.55±37.84 nmol/l; p=0.013. As the MetS score increases, SHBG and HDL levels decrease while weight, BMI, waist circumference, SBP, DBP, FBG, HbA1c, TC, and TG levels increase. SHBG correlated with age, BMI, TG, HDL, TT, free testosterone, and bio-available testosterone. This is the first study that provides detailed analyses of SHBG with MetS components in male diabetic subjects. The mean serum SHBG levels gradually declined with the addition of MetS components in T2D men. TT, free testosterone, and bio-available testosterone remained independently associated with SHBG by multivariable regression analysis.

Alterations in pancreatic milieu to adapt to physiological shifts occurring in conditions of obesity and metabolic syndrome (MS) have been documented, though mechanisms leading to such a state have remained elusive so far. The data presented here tries to look at the gravity of metabolic insult during the early and prolonged phases of obesity/insulin resistance (IR) depicted in WNIN/Ob strain of rats—an obese euglycemic mutant rat model developed indigenously at our institute which is highly vulnerable for a variety of degenerative diseases. The present resultsin situshow the participation of several confounding factors in the pancreatic milieu that collectively coprecipitates for a state of profound inflammation in the pancreas (among Mutant compared to Lean/Control) which gets worsened with age. These include hypertrophy, macrophage infiltration (CD11b/TNFα/IL6), apoptosis,β-cell vacuolation, hyperinsulinemia (HI), and stress markers (RL-77/HSP104/TBARS) all of which correlated well with indices for obesity (2-3 fold), IR (1.5-3 fold), and HI (2-3 fold). Further, supportive data was also obtained fromin vitrostudies using islet cell cultures amongst phenotypes. Taken together, these results advocate that inflammation was the major precipitating factor to cause islet cell dysfunctions (in situandin vitro) in these Mutant rats compared to their Lean littermates and parental Control.

Adiponectin and resistin are adipose tissue-derived proteins with antagonistic actions; adiponectin has insulin sensitive properties while resistin is involved in the development of insulin resistance. We analyzed adiponectin and resistin levels in gestational diabetes mellitus (GDM) women to evaluate the association of these adipokines in a very high diabetes prevalence population. An age-matched case-control study of GDM and normal pregnant women in Saudi population. We recruited 90 pregnant women at 24–32 weeks of gestation. Glucose levels (fasting, 1, 2, and 3 h) and lipid parameters (cholesterol, triglyceride, HDL cholesterol, LDL cholesterol) were measured. Serum adiponectin and resistin levels were analyzed using Randox evidence biochip analyzer. Pearson’s correlation coefficient was used to determine the association of adiponectin and resistin with GDM risk factors. GDM women showed significantly low adiponectin and high resistin levels when compared with control group. Pearson’s correlation analysis of adiponectin and resistin in all the subjects with various GDM risk factors showed a negative association of adiponectin (r = −0.32, p = .05) and a positive correlation of resistin (r = 0.41, p = .01) with LDL cholesterol. This study analyzes adiponectin and resistin levels together, as accumulating evidences shows that these are involved in the pathophysiology of GDM. This is going to help to determine in conjunction with traditional risk factors the incremental value of circulating adiponectin and resistin in developing GDM.