Metabolic diseases such as obesity and diabetes have been the most serious social and health problems in the world. Current treatments mainly focus on the disease consequence rather than the cause of metabolic disorders, and it is difficult to curb the global trend of explosive growth of patients. Thus new and more effective prevention and treatment strategies are needed. Genetics and environment influence the process of obesity and diabetes. But the genomic analysis only accounts for 10% to 20% of the metabolic diseases, while environmental factors such as diet and other lifestyle habits play an important role in the onset of metabolic diseases. In recent years, an increasing number of studies have shown that human gut microbiota is closely related to the onset and development of metabolic diseases such as obesity and type 2 diabetes. The rapid progress in this emerging academic field will not only help elucidate the pathogenesis of metabolic disease, but will also provide direction for exploring new therapeutic targets and pathways.

Incretin hormones are defined as intestinal hormones released in response to nutrient ingestion,and potentiate the glucose-induced insulin response. In humans, the incretin effect is mainly caused by two peptidehormones, glucagon-like peptide-1 ( GLP-1 ) and glucose-dependent insulin releasing polypeptide (GIP). According to the recently finished studies, the review focuses on the physiological actions of incretin, explains the different insulinotropic actions of GLP-1 and GIP in type 2 diabetic patients, and evaluates the clinical features of recently approved therapeutic agents based on incretin action.

Incretin is defined as an intestinal hormone released in response to nutrient ingestion, which potentiates the glucose-induced insulin response. In human body, the incretin's effect is mainly induced by two peptide hormones, glucagon-like peptide-I (GLP-I)and glucose-dependent insulinotropic polypeptide (GIP). In order to fully evaluate the clinical advantages of novel agents based on incretin, this review introduces the islet actions of incretin in brief, and mainly focuses on the extra-islet effect of incretin.

[Summary] MS ,which is highly related tothe occurrence of cardiovascular disease and T2DM ,is characterized by glucose and fat metabolic dysregulation ,central obesity ,hypertension and hyperuricemia.11β‐hydroxysteroid dehydrogenase type 1 (11β‐HSD1) is regarded as a new therapeutic target for MS.11β‐HSD1 converts inactive glucocorticoid to active glucocorticoid. 11β‐HSD1 knockout improves obesity , hyperlipidemia andhyperglycemia. The inhibition of 11β‐HSD1 alleviates IR in human and rodents ,but the application of 11β‐HSD1 inhibitors is limited by the side effects.

Objective To investigate the prevalence and risk factors of diabetic retinopathy(DR) in Chinese elderly diabetic patients. Methods One hundred and ninety patients with type 2 diabetic aged 60 years and over,including 93 males and 97 females were selected.The average age was 68.9 years and the average diabetic duration was 11.5 years.HbA1c,insulin,C-peptide and other clinical characteristics in all patients were tested.The retinopathy of the patients were examined by the retina-camera. Results There were 103 patients without deabetic retinopathy,59 patients carrying nonproliferative deabetic retinopathy and 28 patients carrying proliferative diabetic retinopathy.The above three groups had statistically different diabetic duration((121.1?93.2) vs(149.6?112.1) vs(182.2?83.5)months,P

Objective To investigate the effect of metformin on thyroid hormone and thyrotropin(TSH) in diabetic patients without thyroid hormone replacement.Methods Serum levels of free T3(FT3),free T4(FT4),total T3(TT3),total T4(TT4) and TSH were measured in diabetic patients with or without metformin therapy and the relationship between TSH and metformin was analyzed.Results There were no significant differences in serum FT3(4.65?0.68 vs 4.59?0.67 pmol/L),FT4(17.88?3.26 vs 17.75?2.85pmol/L),TT3(1.79?0.42 vs 1.77?0.38nmol/L),TT4(107.9 ?22.1 vs 109.2?22.1nmol/L) and thyrotropin(ln TSH:0.49?0.83 vs 0.47?0.87 mU/L) between diabetic patients taking and not taking metformin.Conclusions In diabetic patients without thyroid hormone replacement,metformin does not suppress serum TSH.

T polymorphism and early onset familial type 2 diabetes,the frequency of allele T of early onset familial type 2 diabetes population was significantly lower ,and the frequency of allele C significantly higher, than those of control subjects(PT polymorphism at MODY2 gene, intron 9 or nearby genes was associated with early onset familial type 2 diabetes .

HbA1c has already been one of the standard diagnostic criteria for diabetes and pre-diabetes.However,disorders of iron metabolism could affect glucose metabolism through various pathways,and influence HbA1c level directly or indirectly.So under certain circumstances,it may affect the diagnosis of glucose metabolic status.Here we reviewed researches about the interference of iron metabolism disorders on HbA1c.

Objective To explore the association of serum uric acid level with the different states of glucose metabolism and glomerular filtration rate (GFR) reflected by creatinine clearance rate and to test the hypothesis that increased GFR is one of the determinants of serum uric acid level. Methods 822 subjects with high risk factors for diabetes in Beijing area underwent a 75g oral glucose tolerance test (OGTT) for screening of diabetes. The subjects were divided into three groups:NGT,IGR and DM after OGTT. SUA and Ccr were compared between three groups. The general linear model was employed to test the relationships of the small FPG intervals with SUA and Ccr. Results The correlations of uric acid level with sex,BMI,TG,HbA1c and Ccr remained significant in a multiple regression analysis. After adjusting sex,BMI and TG,the newly diagnosed DM group had the lowest SUA level(P

Objective To investigate the clinical characteristics of the familial early onset type 2 diabetes（T2DM）,and the factors affecting the age at diagnosis. Methods 190 probands from early onset T2DM pedigrees （diagnosed before 40 years old） and 103 probands from late onset T2DM （pedigrees） （all patients were diagnosed after 40 years old）were included in this study. The homeostasis model assessment of insulin resistance （HOMA-IR）was used to estimate insulin resistance, HOMA-β cell was used to evaluate basal insulin secretion. The ratio of the incremental insulin (ΔI30) over （incremental） glucose(ΔG30) was calculated after intake of a steamed bread made of 100g flour to （evaluate） the early insulin secretion. Body mass index（BMI）and serum lipid levels were also （determined.） （Results） （1）The early onset group had significantly higher fasting serum insulin （（natural） logarithm transformed, 2.6±0.6 vs 2.4±0.5 μU/ml, P<0.05）, triglycerid （TG, 1.7±2.0 vs 1.4±2.0 mmol/L,P<0.05）,HOMA-IR（natural logarithm transformed, 1.6±0.8 vs 1.3±0.6, P<0.01）and lower high density lipoprotein （HDL-C, 1.2±0.3 vs 1.3±0.3mmol/L,P<0.05） than those in late onset group.（2）Linear regression analyses showed that HOMA-IR, HOMA-β were （independent） risk factors predicting early age of onset. （3）In the early onset type 2 diabetic patients, the subgroup with BMI more than 25 kg/m2 had significant earlier diagnosis age （32±7 vs 34±5 y, P<0.05）, lower level of serum HDL-C （1.1±0.3 vs 1.3±0.3 mmol/L, P<0.01）, higher FIns （（natural） logarithm transformed, 2.8±0.6 vs 2.4±0.6, P<0.01）, higher HOMA-IR （natural （logarithm） transformed, 4.3±0.9 vs 3.9±1.0, P<0.01）and higher TG （1.9±2.0 vs 1.5±2.1 mmol/L, P<0.01）than those with BMI less than 25 kg/m2. Conclusion Compared with late onset familial type 2 diabetic patients,more severe insulin resistance and relative β cell function defect are the important clinical （features） in early onset familial type 2 diabetic patients. The interaction between （insulin resistance） and （β-cell） dysfunction are probably the determinants of onset age of T2DM.