Adiponectin has multiple functions including insulin sensitization, anti-inflammation and antiatherogenesis in various organs. Adiponectin activates 5′-adenosine monophosphate-activated protein kinase (AMPK) and peroxisome proliferator-activated receptor (PPAR)α via the adiponectin receptor (AdipoR) 1 and 2, which are critical for regulating lipids and glucose homeostasis and for controlling oxidative stress. We investigated whether resveratrol can inhibit renal damage in type 2 diabetic db/db mice and the underlying mechanisms of its effects. Four groups of male C57 BLKS/J db/m and db/db mice and human glomerular endothelial cells (HGECs) were used. Resveratrol was administered to diabetic and nondiabetic mice by oral gavage for 12 weeks starting at 8 weeks of age. In db/db mice, resveratrol increased serum adiponectin levels and decreased albuminuria, glomerular matrix expansion, inflammation and apoptosis in the glomerulus. Resveratrol increased the phosphorylation of AMPK and silent information regulator T1 (SIRT1), and decreased phosphorylation of downstream effectors class O forkhead box (FoxO)1 and FoxO3a via increasing AdipoR1 and AdipoR2 in the renal cortex. Furthermore, resveratrol increased expression of PPARγ coactivator (PGC)-1α, estrogen-related receptor-1α, and phosphorylated acetyl-CoA carboxylase and decreased sterol regulatory element-binding protein 1. This effect lowered the content of nonesterified fatty acid and triacylglycerol in the kidneys, decreasing apoptosis, oxidative stress and activating endothelial nitric oxide synthase. Resveratrol prevented cultured HGECs from undergoing high-glucose-induced oxidative stress and apoptosis by activating the AMPK–SIRT1–PGC–1α axis and PPARα through increases in AdipoR1 and AdipoR2 expression. These results suggest that resveratrol prevents diabetic nephropathy by ameliorating lipotoxicity, oxidative stress, apoptosis and endothelial dysfunction via increasing AdipoR1 and AdipoR2 expression.

Hyperuricemia is associated with obesity. The visceral adiposity and subcutaneous adiposity may be associated with the differential metabolic risk, and the distribution of abdominal adipose tissue was significantly altered in people with type 2 diabetes mellitus (DM) compared to healthy people. Our study was performed to determine to the association between the regional abdominal adipose tissue distribution and serum uric acid levels in people with type 2 DM. A total of 699 people with type 2 DM and who had undergone abdominal computed tomography assessment of the visceral fat area and subcutaneous fat area were included. The serum uric acid levels were measured by the uricase method. Hyperuricemia was defined by cut-off value of > 7 mg/dl for men and > 6 mg/dl for women. The visceral fat area was positively associated with the serum uric acid levels after adjustment for age, sex, systolic blood pressure, diastolic blood pressure, serum creatinine, hemoglobin, serum albumin, serum high-density lipoprotein, serum triglyceride and hemoglobin A1c (β-coefficient = 0.117, p < 0.001). The logistic regression analysis showed that the visceral fat area was the significant independent predictor of hyperuricemia (OR 2.33, 95% CI, 1.21-4.50, p = 0.012). But there was no significant association between the subcutaneous fat area and the serum uric acid levels (β-coefficient = 0.061, p = 0.255). our data shows that the visceral fat area was positively associated with the serum uric acid levels, but the subcutaneous fat area was not in people with type 2 DM.

Hyun YY, et al. J Korean Med Sci. 2017 Feb;32(2):257-263. https://doi.org/10.3346/jkms.2017.32.2.257

Myostatin, a member of the transforming growth factor-β (TGF-β) superfamily, is a potent negative regulator of skeletal muscle growth. The objective of this study was to produce a monoclonal anti-myostatin antibody and to examine the effects of in ovo administration of the antibody on posthatch broiler growth and muscle mass. The mature form of myostatin was expressed in Escherichia coli and used as an immunogen in producing a monoclonal antibody against myostatin. One hybridoma clone (mAb-c134) that showed the strongest affinity to the immunogen in Western blot analysis was used in producing a large quantity of monoclonal anti-myostatin antibody. In Western blot analysis, this antibody showed a strong binding affinity to commercially available mature myostatin and demonstrated a certain level of crossreactivity with recombinant human BMP2 but not withrecombinant human TGF-β3 or porcine TGF-β1. Competitive ELISA demonstrated binding of the antibody to the native form of mature myostatin in solution. To examine the effects of in ovo administration of the mAb-c134 antibody, eggs were injected once with 40 µg of mAb-c134 in 50 mL of PBS either into the albumen or yolk on d 3 of incubation. Controls received no injection. After hatching, chicks were raised for 35 d. Broilers from eggs that had the antibody injected into the yolk had significantly heavier body (4.2%) and muscle (5.5%) mass than the controls in both male and female birds. In contrast, no significant effects on body and muscle mass were observed when the mAb-c134 antibody was injected into the albumen. The results of this study suggest that immunoneutralization of myostatin during embryonic development is a potential means to improve growth potential of broilers.

Kang E, et al. J Korean Med Sci. 2017 Feb;32(2):221-230. https://doi.org/10.3346/jkms.2017.32.2.221