Objective To investigate correlation of abdominal adipose tissue distribution and insulin resistance in T2DM. Methods A total of 128 T2DM patients were divided into two groups :obese (OG) group (n=66) and non‐obese (NOG) group (n=62). Spiral CT was used for the measurement of adipose tissue of the total area (TA) and visceral fat area (VA) at abdominal umbilical level lumbar vertebrae 4 ,5 plane in T2DM patients. Subcutaneous fat area (SA ) was calculated. General and biochemical characteristics were measured in both groups. Results WC [male(73.52 ± 0.88) vs (70.66 ± 0.92)cm ;female(83.22 ± 0.96) vs (78.98 ± 0.98)cm] ,BMI [male(28.85 ± 3.45) vs (25.11 ± 4.36)kg/m2 ;female (28.23 ± 3.48) vs (25.05 ± 3.89)kg/m2 ] ,SBP [male(158.23 ± 8.25) vs (112.25 ± 7.25)mmHg ;female (154.25 ± 6.32) vs (109.68 ± 8.02)mmHg] ,DBP [male(95.36 ± 5.26) vs (80.69 ± 7.25)mmHg ;female (92.45 ± 4.36) vs (80.26 ± 6.48)mmHg] ,FPG [male(9.85 ± 2.89) vs (7.03 ± 2.88)mmol/L ;female (9.75 ± 2.65) vs (7.39 ± 2.98)mmol/L] ,FIns [male(11.25 ± 3.45) vs (7.02 ± 2.43)mIU/L ;female (11.02 ± 3.58) vs (7.18 ± 2.69)mIU/L] ,HbA1c [male(7.36 ± 1.36)% vs (5.21 ± 0.37)% ;female(7.68 ± 1.22)% vs (5.32 ± 0.42)% ] ,TG [male(5.98 ± 1.52) vs (3.02 ± 0.89)mmol/L ;female(5.78 ± 1.26) vs (2.98 ± 0.92)mmol/L] ,TC [male(8.02 ± 1.28) vs (4.39 ± 0.98)mmol/L ;female(7.98 ± 1.13) vs (4.23 ± 0.89)mmol/L] ,LDL‐C [male(9.12 ± 0.58) vs (4.21 ± 0.86)mmol/L ;female(8.96 ± 0.78) vs (4.18 ± 0.92)mmol/L] ,SUA [male(83.63 ± 21.64) vs (72.98 ± 12.25)μmol/L ;female(83.98 ± 19.78) vs (71.98 ± 11.98)μmol/L] ,C‐RP [male(5.96 ± 1.25) vs (2.32 ± 0.42)mg/L ;female(5.05 ± 1.32) vs (2.52 ± 0.56)mg/L] ,HOMA‐IR [male(4.25 ± 1.12) vs (2.25 ± 1.12);female(4.36 ± 1.42) vs (2.12 ± 1.02)] ,TA [male(50.68 ± 9.12) vs (30.96 ± 3.26)cm2 ;female(47.23 ± 4.23) vs (26.98 ± 3.02)cm2 ] , VA [male(19.78 ± 5.42) vs (10.59 ± 4.69)cm2 ;female(17.02 ± 3.96) vs (8.45 ± 3.78)cm2 ] ,SA [male (30.91 ± 6.02) vs (18.96 ± 5.78)mm2 ;female(28.25 ± 4.23) vs (17.25 ± 4.62)mm2 ]and VA/SA [male (0.72 ± 0.22)% vs (0.42 ± 0.18)% ;female(0.58 ± 0.17)% vs (0.32 ± 0.12)% ] were significantly higher in OG group than in NOG group. T2DM course [male(2.36 ± 0.58) vs (2.62 ± 0.78)years ;female (2.38 ± 0.62) vs (2.82 ± 0.82)years] ,HDL‐C [male(0.98 ± 0.21) vs (2.28 ± 0.78)mmol/L ;female(0.96 ± 0.32) vs (2.19 ± 0.82)mmol/L] and HOMA‐β[male(28.22 ± 9.34) vs (82.22 ± 31.25);female(28.02 ±8.02) vs (81.36 ± 28.36)] were lower in OG group than in NOG group(P< 0.05). Spearson correlation analysis showed that HOMA‐IR was positively associated with TG ,SUA ,TA ,VA ,SA ,VA/TA ,SA/TA and VA/SA. Logistic multiple regression analysis showed that TG ,SA ,TA and VA/TA were risk factors for insulin resistance in T2DM patients. Conclusion Abdominal fat distribution is closely related to IR in T2DM patients.

Objective To investigate the molecular mechanism of metformin. Methods The changes of protein expression of IRS-1 in liver, skeletal muscle and adipose tissues after treatment with metformin for OLETF rats, a model of spontaneous type 2 diabetes mellitus, were measured by Western blot analysis, and compared with those before treatment. Results 22 weeks after the treatment with metformin, the protein expression of IRS-1 was significantly increased in liver (P0. 05) ;and the protein expression of IRS-1 in adipose tissue was significantly decreased (P

The levels of protein expressions o f insulin receptor substrate-1 and -2 (IRS-1 and IRS-2) in abdominal subcuta neous adipose tissue from type 2 diabetic patients were measured by Western blot technique. The expression of IRS-1 protein was reduced and the expression of I RS-2 protein was unchanged in adipose tissue of type 2 diabetic patients. IRS- 2 may be the main docking protein and one of the factors causing hyperinsulinemi a and insulin resistance in type 2 diabetes mellitus.

Glomerular hyperfiltration(GHF), as an early manifestation of prediabetes and diabetic kidney disease, occurs mainly by the mechanism of glomerular-tubular feedback and hemodynamic alterations, and the risk of hyperfiltration can be elevated in younger patients, shorter duration of the disease, poor glycemic control, and high-protein, low-salt diet. Currently, there is no recognized standard for the definition of GHF, GHF lacks typical clinical manifestations, imaging diagnostic criteria are unclear, and GHF-related laboratory markers need to be further studied. Hyperfiltration, if not diagnosed and intervened in time, can accelerate the damage of nephron and the rate of nephropathy progression, and increase the risk of complications and death. Sodium-glucose cotransporter 2 inhibitor(SGLT2i), glucagon-like peptide-1 receptor agonist(GLP-1RA)and so on can effectively reverse the hyperfiltration state. Clinical attention should be paid to the diagnosis of diabetic hyperfiltration and the prevention of its poor prognosis.

Glomerular hyperfiltration(GHF), as an early manifestation of prediabetes and diabetic kidney disease, occurs mainly by the mechanism of glomerular-tubular feedback and hemodynamic alterations, and the risk of hyperfiltration can be elevated in younger patients, shorter duration of the disease, poor glycemic control, and high-protein, low-salt diet. Currently, there is no recognized standard for the definition of GHF, GHF lacks typical clinical manifestations, imaging diagnostic criteria are unclear, and GHF-related laboratory markers need to be further studied. Hyperfiltration, if not diagnosed and intervened in time, can accelerate the damage of nephron and the rate of nephropathy progression, and increase the risk of complications and death. Sodium-glucose cotransporter 2 inhibitor(SGLT2i), glucagon-like peptide-1 receptor agonist(GLP-1RA)and so on can effectively reverse the hyperfiltration state. Clinical attention should be paid to the diagnosis of diabetic hyperfiltration and the prevention of its poor prognosis.