Key result
Visceral adiposity in non-obese T2DM links to lower HMW adiponectin, higher CRP, and greater insulin resistance.
Why the study?
Does visceral adiposity affect adiponectin levels, inflammation, and insulin resistance in non-obese Japanese patients with type 2 diabetes?
Observational (n=138)
Does visceral adiposity affect adiponectin levels, inflammation, and insulin resistance in non-obese Japanese patients with type 2 diabetes?
Visceral fat accumulation is associated with decreased adiponectin, increased inflammation, and increased insulin resistance in non-obese patients with type 2 diabetes, suggesting an increased cardiovascular risk profile.
May flag higher CV risk in non-obese T2D; hypothesis-generating and should not yet change practice.
Objective: Visceral fat accumulation because of obesity plays a central role in metabolic syndrome and causes cardiovascular disease (CVD). Methods: The aims of this study were to investigate associations between visceral fat accumulation and adipokines in non-obese type 2 diabetic patients. Results: In total, 138 type 2 diabetic patients were enrolled, with a mean age of 64 years. Among the participants, 69 were males. We found that serum high-molecular-weight adiponectin level was decreased, C-reactive protein increased, and using homeostatic model assessment of insulin resistance was also increased in non-obese patients with visceral adiposity (body mass index: BMI, <25 kg/m2; visceral fat area: VFA, ≥ 100 cm2) compared with those without visceral adiposity (BMI, <25 kg/m2, VFA, <100 cm2). VFA in non-alcoholic fatty liver disease (NAFLD) was higher than in those with no NAFLD. Conclusion: We demonstrated that visceral fat accumulation is a risk for CVD in non-obese diabetic patients with visceral adiposity.
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Yamada et al. (2016) conducted an observational in Type 2 diabetes (n=138). Visceral adiposity (BMI <25 kg/m2, VFA ≥ 100 cm2) vs. No visceral adiposity (BMI <25 kg/m2, VFA <100 cm2) was evaluated on Serum high-molecular-weight adiponectin, C-reactive protein, and HOMA-IR. Visceral adiposity in non-obese type 2 diabetic patients was associated with decreased high-molecular-weight adiponectin, increased C-reactive protein, and increased insulin resistance.
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