803-P: Serum Adiponectin Level Is Reduced after Short-Term Intensive Insulin Therapy in Patients with Newly Diagnosed Type 2 Diabetes

Abstract

Objective: Short-term intensive insulin therapy (SIIT) can induce remission of type 2 diabetes (T2D) , and the improvement of insulin sensitivity is considered essential. This study aimed to evaluate the role of adiponectin change during SIIT in patients with newly diagnosed T2D. Methods: SIIT was given to 42 patients with newly diagnosed T2D to normalize blood glucose (4.4-6.0 mmol/L for fasting blood glucose [FBG], 4.4-8.0 mmol/L for 2h-postprandial blood glucose [2hBG]) for two weeks. Serum lipids, adiponectin, and high-sensitive C reactive protein levels, insulin resistance and β-cell function were evaluated before and after SIIT. Results:After the therepy, FBG (11.8±2.9 mmol/L vs. 6.8±1.3mmol/L,P<0.001) and 2hPG (18.4mmol/L± 6.4mmol/L vs. 9.7±2.4mmol/L, P<0.001) were both significantly decreased, with β-cell function (measured by acute insulin response [AIR], HOM-B) and insulin sensitivity (measured by HOMA-IR) improved. Serum adiponectin raised from 2.9±1.2mg/L to 3.4±1.1mg/L (P<0.001) ,while serum triglyceride and LDL-C decreased significantly. Serum adiponectin after treatment was correlated with baseline triglyceride (r = -0.33, P = 0.04) , HDL-C (r = 0.34, P = 0.03) , LDL-C (r = -0.31, P = 0.05) and Hs-CRP (r = -0.33, P = 0.05) ; the change of adiponectin (Δadiponectin) after treatment were significantly correlated with the level of Δtriglyceride (r = 0.38, P = 0.03) . There was no notable correlation between adiponectin and β-cell function index or HOMA-IR. Adiponectin levels were similar between patients who obtained diabetes remission (defined as FBG< 7.0mmol/L, 2hBG<10.0mmol/L without hypoglycemic agents) and those who did not (baseline:3.0±1.5mg/L vs. 2.9±1.0 mg/L; after SIIT:3.4±1.0mg/L vs. 3.3±0.9 mg/L,both P>0.05) . Conclusion: Adiponectin level was significantly increased after SIIT in patients with newly diagnosed T2D. The change of adiponectin is related to the improvement of lipid metabolism and reduced inflammation. Disclosure L.Liu: None. W.Ke: n/a. J.Chen: None. Y.Li: None. Funding The National Key R&D Program of China (2018YFC1314100) , the Key-Area Research and Development Program of Guangdong Province (2019B020230001) , the National Natural Science Fund of China (81800716) , the science and technology program of Guangzhou, 202002020053.