Higher BMI and lower femoral neck strength in males with type 2 diabetes mellitus and normal bone mineral density.

BACKGROUND: Type 2 diabetes mellitus (T2DM) and osteoporosis are two age-associated diseases. Body mass index (BMI) is positively associated with osteoporosis or osteopenia in T2DM population. Bone mineral density does not necessarily reflect the alterations in bone microarchitecture. Our aims were to investigate the relationship between BMI and femoral neck strength in males with T2DM and normal range of bone mineral density (BMD). METHODS: This study enrolled 115 males (median age 53.3 years) with T2DM and normal BMD. Femoral neck strength indexes, including compression strength index (CSI), bending strength index (BSI), impact strength index (ISI), were calculated by parameters generated from Dual-energy X-ray absorptiometry software. Pearson correlation analysis was performed to evaluate the relationships between BMI and femoral neck strength variables. RESULTS: Compared with T2DM-normal weight group, T2DM-overweight group and T2DM-obesity group had a higher femur neck and total femur BMDs. Cross sectional moment of inertia (CSMI), cross sectional area (CSA), section modulus (SM) were significantly higher (all p<0.05), and buckling ratio (BR) (6.35±2.08 vs 7.18±1.71) was lower in T2DM-obesity group than in T2DM-normal weight group. Compared with T2DM-normal weight group, CSI (all p<0.001), BSI (all p<0.001), ISI (all p<0.001) were significantly reduced in T2DM-obesity and T2DM-overweight groups. Pearson correlation analysis indicated that BMI was negatively correlated with CSI (r= - 0.457, p<0.001), BSI(r = -0.397, p<0.001), ISI (r = - 0.414, p<0.001). CONCLUSIONS: Higher BMI is associated with lower femoral neck strength in males with T2DM and normal BMD. It implies that femoral neck fracture risk increases in obese and diabetic males, despite their high bone density.

Elevated serum pentosidine is independently associated with the high prevalence of sarcopenia in Chinese middle-aged and elderly men with type 2 diabetes mellitus.

AIMS/INTRODUCTION: Sarcopenia has recently been recognized as another complication associated with diabetes, but its early screening still lacks clinical markers. Here, we aimed to investigate the relationship between serum levels of pentosidine, which is an advanced glycation end-product, and sarcopenia in Chinese middle-aged and elderly men with type 2 diabetes mellitus and evaluate whether pentosidine could be used as a kind of screening maker. MATERIALS AND METHODS: A total of 182 male type 2 diabetes mellitus patients aged ≥50 years were selected in the cross-sectional study for whole-body dual-energy X-ray measurement and calculating the appendicular skeletal muscle mass index. At the same time, handgrip strength and gait speed were assessed. According to the updated consensus on Asian sarcopenia in 2019, the patients were divided into the sarcopenia group (n = 83) and non-sarcopenia group (n = 99). Serum pentosidine levels in the two groups were detected using enzyme-linked immunosorbent assay. RESULTS: Serum pentosidine was significantly higher in the sarcopenia group (191.27 pmol/mL) than in the non-sarcopenia group (34.93 pmol/mL). Serum pentosidine was negatively correlated with appendicular skeletal muscle mass index and handgrip strength (r = -0.30 and -0.25, respectively; P < 0.05), but not gait speed. The prevalence of sarcopenia increased as the quartile of serum pentosidine increased (P < 0.05). The association between pentosidine and the prevalence of sarcopenia was still significant after additional adjustments (odds ratio 1.01, P < 0.05). CONCLUSIONS: Pentosidine is an independent risk factor for sarcopenia in Chinese middle-aged and elderly men with type 2 diabetes mellitus. The detection of serum pentosidine levels in clinics might be helpful for the monitoring of type 2 diabetes mellitus complicated with sarcopenia.

A combination of plasma exchange and steroids in the treatment of a-lipoic acid-induced insulin autoimmune syndrome.

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Inverse relationship between serum Metrnl levels and visceral fat obesity (VFO) in patients with type 2 diabetes.

AIM: The relationship between serum Metrnl levels and visceral fat obesity (VFO) remains unclear. This study aimed to investigate the association between serum Metrnl levels and VFO in Chinese patients with type 2 diabetes. METHODS: A total of 321 Chinese patients with type 2 diabetes (226 men and 95 postmenopausal women aged 61.4 ± 6.5 years, BMI 25.1 ± 3.2 kg/m2) were evaluated. Serum Metrnl levels were measured by enzyme linked-immunosorbent assay. Visceral fat area (VFA) was quantified via Dual Energy X-ray Absorptiometry (DXA). Correlation analyses were carried out for serum Metrnl levels and VFO. RESULTS: VFO groups (VFA ≧100 cm2) have lower serum Metrnl levels than non-VFO groups (VFA < 100 cm2) (578.9 ± 225.1 vs. 684.9 ± 263.8, P = 0.001). An increasing trend in serum Metrnl levels was found to accompany the decrease in VFA. Serum Metrnl levels were negatively correlated with VFA, total cholesterol (TC), triglyceride (TG), low-density lipoprotein cholesterol (LDL-C) and albumin (ALB), but positively correlated with age, height, blood urea nitrogen (BUN), creatinine (Cr) and uric acid (UA) (all P < 0.05). Binary logistic regression analysis showed that serum Metrnl was inversely associated with VFO even after adjusted age, gender, height, TC, TG, LDL-C, ALB, BUN, Cr, and UA (odds ration [OR], 0.846; confidence interval [CI], 0.745-0.961; P = 0.010). The optimal cut-off value of serum Metrnl levels that predicted VFO was 671.3 ng/ml (95%CI = 0.55-0.70, P = 0.001). CONCLUSIONS: Serum Metrnl levels were inversely correlated with VFO and may be a useful indicator of VFO in Chinese patients with type 2 diabetes.

Egr2 enhances insulin resistance via JAK2/STAT3/SOCS-1 pathway in HepG2 cells treated with palmitate.

Insulin resistance is generally responsible for the pathogenesis of type 2 diabetes mellitus (T2DM). Early growth response proteins-2 (Egr2) has been reported to be able to increase the expression of the suppressors of cytokine signaling-1 (SOCS-1), and impair insulin signaling pathway through suppression of insulin receptor substrates (IRS), including IRS-1 and IRS-2. However, whether Egr2 is directly involved in the development of insulin resistance, and how its potential contributions to insulin resistance still remain unknown. Here, our present investigation found that the expression levels of Egr2 were up-regulated when insulin resistance occurs, and knockdown of Egr2 abolished the effect of insulin resistance in HepG2 cells induced with palmitate (PA). Importantly, inhibition of Egr2 decreased the expression of SOCS-1 as well as reduced phosphorylation of JAK2 and STAT3. And, our data indicated that silencing of Egr2 accelerated hepatic glucose uptake and reversed the impaired lipid metabolism upon insulin resistance. In summary, the present study confirms that Egr2 could deteriorate insulin resistance via the pathway of JAK2/STAT3/SOCS-1 and may shed light on resolving insulin resistance and further the pathogenesis of T2DM.