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Periostin, as an emerging biomarker, is involved in multiple steps in bone metabolism. This study aimed to investigate the correlation between periostin levels and bone mineral density as well as bone turnover markers in postmenopausal women with type 2 diabetes (T2DM).This study was a cross-sectional study that included 164 postmenopausal women with T2DM as study subjects and 32 age-matched nondiabetic postmenopausal women with normal bone mineral density (BMD) as healthy control subjects. A total of 164 subjects with T2DM were then divided into three groups according to BMD: the normal BMD group (n = 29), the osteopenia group (n = 70), and the osteoporosis group (n = 65). The clinical data of all subjects along with the relevant biochemical parameter data were collected. Plasma periostin was detected using an enzyme-linked immunosorbent assay (ELISA).Plasma periostin levels were significantly increased in T2DM patients with normal BMD compared with healthy controls (p 0.05). In the diabetic group, plasma periostin levels were significantly elevated with decreased BMD, were positively correlated with osteocalcin levels (r = 0.162, p = 0.039) and were inversely associated with femoral neck BMD (r = - 0.308, p 0.001) and total femur BMD (r = - 0.295, p 0.001). In the case of chronic complications, periostin levels were slightly increased in individuals with complications of diabetic retinopathy, diabetic nephropathy and fracture (p 0.05).The current study demonstrated that plasma periostin levels were significantly associated with BMD in patients with T2DM, and periostin might act as a novel biochemical marker of osteoporosis in postmenopausal women with type 2 diabetes.

As a major health issue, obesity is linked with elevated risk of type 2 diabetes. However, whether disrupted glucose homeostasis is due to altered body composition alone, or whether dietary macronutrients play an additional role, independent of their impact on body composition, remains unclear. We investigated the associations between macronutrients, body composition, blood hormones and glucose homeostasis. We fed C57BL/6N mice 29 different diets with variable macronutrients for 12 weeks. After 10 weeks, intraperitoneal glucose tolerance tests were performed. Generalized linear models were generated to evaluate the impacts of macronutrients, body composition and blood hormones on glucose homeostasis. The area under the glucose curve (AUC) was strongly associated with body fat mass, but not dietary macronutrients. AUC was significantly associated with fasting insulin levels. Six genes from transcriptomic analysis of epididymal white adipose tissue and subcutaneous white adipose tissue were significantly associated with AUC. These genes may encode secreted proteins that play important previously unanticipated roles in glucose homeostasis., Hu et al. found that disrupted glucose homeostasis in obese mice is mainly due to high body fatness, and dietary fat plays an additional role on fasting glucose levels.

Early predication and intervention of diabetic nephropathy is increasingly imperative. Hyperhomocysteinemia is common and chronically induces arteriolar thickening, and tubulointerstitial and podocyte injury, therefore, could play a causative role in early renal injury in the kidney in type 2 diabetes. In this study, we for the first time investigated the relation of plasma total homocysteine concentration to early nephropathy in type 2 diabetes. We enrolled 183 type 2 diabetic patients in a cross-sectional study. Early diabetic nephropathy status was diagnosed by presence of microalbuminuria. Plasma total homocysteine levels were measured using fluorescence polarization immunoassay. Variables for diabetic nephropathy were obtained from fasting blood samples and interviewer- questionnaire. We found that plasma total homocysteine concentrations were elevated in subjects with early diabetic nephropathy than without (13.3±2.9)µmol/l vs. (8.5 ± 1.4)μmol/l, p < 0.01). The association of homocysteine with the diabetic nephropathy was independent of major traditional risk factors for diabetic nephropathy (duration of diabetes, HbA1c, and blood pressure) and determinants of higher homocysteine concentration (age, sex, serum folate and vitamin B12, Biguanide use, and serum cystatin or creatinine levels,) (OR: 1.36 (1.08-1.74), p < 0.05). Furthermore, per increase of 5.0 μmol/l plasma homocysteine was related to early nephropathy (OR: 1.15 (1.04-1.29), p < 0.05), after controlling for per unit increase of other factors: per 5 year increase of duration of diabetes, per 1% increase of HbA1c, per 10 nmol/l increase of serum folate, per 100 pmol/l increase of serum B12, per 0.1 mg/L increase of serum cystatin or per 10 μmol/l increase of creatinine, and per 10 or 5 mmHg increase of systolic or diastolic blood pressure. We concluded that plasma total homocysteine concentration was independently associated with occurrence of early diabetic nephropathy. Future prospective studies are warranted. Disclosure J. Li: None. Q. Lv: None. H. Lu: None. H. Zhang: None. J. Zhou: None. Funding National Natural Science Foundation of China (81070655); Jiangsu Provincial Natural Science Foundation of China (BK2009441)

Macular edema that impairs central vision is one of leading causes of blindness related to diabetes. Hyperhomocysteinemia is more common in type 2 diabetes, which may damage endothelium by excessive sulphation of connective tissues. In this study, we for the first time explored the relation of plasma total homocysteine concentration to diabetic macular edema in patients with type 2 diabetes. We enrolled 176 type 2 diabetic patients and 115 healthy subjects in a cross-sectional hospital-based study. Using fundus photographs documented retina statuses and using fluorescence polarization immunoassay measured homocysteine concentration. Risk factors for diabetic macular edema were obtained from fasting blood samples and interviewer- questionnaire. We found that diabetic patients had increased plasma homocysteine compared with normal control, and plasma homocysteine levels were higher in subjects with diabetic macular edema than without ((11.4 ± 2.7) vs. (8.5 ± 1.9) (μmol/l), p = 0.000). The association of homocysteine with diabetic macular edema was independent of major risk factors for diabetic macular edema (duration of diabetes, HbA1c, lipid) and determinants of higher homocysteine concentration (age, gender, serum folate and vitamin B12, renal status, and biguanide use) (OR: 1.63 (1.02-2.14), p = 0.018). Furthermore, a 1 μmol/l increase in plasma homocysteine concentration was associated with a 0.5% to 2.2% increase of diabetic macular edema and per increase of 5.0 μmol/l plasma homocysteine was significantly related to macular edema (OR: 1.64 (1.04-2.16), p = 0.019) after adjusting for duration of diabetes per 5 year increase, HbA1c per 1% increase, serum folate per 10 nmol/l increase, serum B12 per 100 pmol/l increase, serum creatinine per 10 μmol/l increase and urinary ACR per 5 mg/g increase. We concluded that hyperhomocysteinemia is independently associated with occurrence of macular edema in type 2 diabetes. Future prospective studies are warranted to clarify the relationship. Disclosure J. Li: None. H. Zhang: None. Q. Lv: None. H. Lu: None. J. Zhou: None.

To explore the relationship between plasma total homocysteine concentration and diabetic macular edema in patients with type 2 diabetes.Patients with type 2 diabetes (n = 176) were enrolled in a cross-sectional hospital-based study. Diabetic macular edema status was documented by fundus photographs. Plasma total homocysteine concentration was measured using fluorescence polarization immunoassay. Normal control plasma homocysteine was established in 115 healthy subjects. Risk factors for diabetic macular edema were obtained from fasting blood samples and interviewer questionnaire.Diabetic patients had increased plasma homocysteine compared with normal control. Plasma homocysteine levels were higher in subjects with diabetic macular edema than without ((11.4 ± 2.7) versus (8.5 ± 1.9) (μmol/l), p = 0.000). The association of homocysteine with diabetic macular edema was independent of major risk factors for diabetic macular edema (duration of diabetes, HbA1c, lipid) and determinants of higher homocysteine concentration (age, gender, serum folate and vitamin B12, renal status, and biguanide use) (OR: 1.63 (1.02-2.14), p = 0.018). Furthermore, per increase of 5.0 μmol/l plasma homocysteine was related to macular edema, after controlling for per unit increase of other factors (OR: 1.64 (1.04-2.16), p = 0.019).Plasma total homocysteine concentration is independently associated with the occurrence of macular edema in type 2 diabetes. Future prospective studies are warranted to clarify the relationship.

Aims/Introduction Data on hyperhomocysteinemia in relation to fractures in diabetes are limited. We aimed to explore the relationship between plasma total homocysteine concentrations and fractures in men and premenopausal women with type 2 diabetes. Materials and Methods Diabetic and control participants (n = 292) were enrolled in a cross-sectional hospital-based study. Bone mineral density and fractures were documented by dual energy X-ray absorptiometry and X-ray film, respectively. Plasma total homocysteine concentrations were measured using fluorescence polarization immunoassay. Risk factors for low bone mineral density or fractures and determinants of homocysteine were obtained from blood samples and the interviewer questionnaire. Results Plasma total homocysteine levels were higher in diabetic participants with fractures than without (8.6 [2.1] μmol/L vs 10.3 [3.0] μmol/L, P = 0.000). Diabetic participants with fractures had similar bone mineral densities as control participants. The association of homocysteine with the fracture was independent of possible risk factors for fractures (e.g., age, duration of diabetes, glycated hemoglobin, body mass index, thiazolidenediones and retinopathy) and determinants of homocysteine concentration (e.g., age, sex, serum folate and vitamin B12, renal status and biguanide use; odds ratio 1.41, 95% confidence interval 1.05–2.03, P = 0.020). Furthermore, per increase of 5.0 μmol/L plasma homocysteine was related to the fracture, after controlling for per unit increase of other factors (odds ratio 1.42, 95% confidence interval 1.12–1.78, P = 0.013). Conclusions Plasma total homocysteine concentration is independently associated with occurrence of fractures in men and premenopausal women with type 2 diabetes. Future prospective studies are warranted to clarify the relationship.

AIM To explore the relationship between plasma total homocysteine concentration and diabetic nephropathy in patients with Type 2 diabetes. METHODS Chinese patients with Type 2 diabetes (n = 183) were enrolled in a cross-sectional hospital based study. Early diabetic nephropathy status was documented by presence of microalbuminuria. Plasma total homocysteine concentration was measured using fluorescence polarization immunoassay. Traditional risk factors for diabetic nephropathy were obtained from fasting blood samples and interviewer- questionnaire. RESULTS Plasma total homocysteine levels were higher in subjects with early diabetic nephropathy than without (13.3 ± 2.9) μmol/l vs. (8.5 ± 1.4) μmol/l, p < 0.01). The association of homocysteine with the diabetic nephropathy was independent of major traditional risk factors for diabetic nephropathy (duration of diabetes, HbA1c, and blood pressure) and determinants of higher homocysteine concentration (age, gender, serum folate and vitamin B12, serum cystatin and creatinine levels, and Biguanide use) (OR: 1.37 (0.89 - 2.24), p < 0.05). Furthermore, per increase of 4.0 μmol/l plasma homocysteine was related to nephropathy, after controlling for per unit increase of other factors (OR: 1.15 (0.94 - 1.29), p < 0.05). CONCLUSION Plasma total homocysteine concentration was independently associated with occurrence of early diabetic nephropathy in Chinese patients. Future prospective studies are warranted to clarify the relationship.