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Obesity is strongly associated with insulin resistance, type 2 diabetes, cardiovascular diseases and dyslipidemia. How these seemingly distinctive diseases cluster together as the metabolic syndrome is a scientifically intriguing and clinically important question, but not well understood. Recent studies indicate that chronic systemic inflammation may be a cause behind the syndrome and that the adipose tissue may contribute to the inflammation since it is not only a storage depot for excess fat, but also is an endocrine organ secreting many polypeptides, known as adipokines. Dysregulation of adipokines may be responsible for the elevation of the inflammatory state in obesity and obesity-associated comorbidities. Numerous studies have investigated the change of adipokines in obesity and diabetes conditions, but the data from Chinese patients are very limited. In this study, we measured the serum levels of several representative adipokines in obese and diabetic Chinese patients treated with rosiglitazone. In non-diabetic subjects, the serum levels of serum amyloid A (SAA), C-reactive protein (CRP) and TNFa in obese people (BMI ≥ 24, n = 24) was significantly higher than the lean subjects (BMI < 24, n = 26, p < 0.01). In contrast, adiponectin levels were significantly lower in the obese group (p < 0.01). On the other hand, no difference in IL-6 and resistin levels was found between the lean and obese groups. Moreover, these adipokines were measured in 34 impaired glucose regulation (IGR) patients and 44 new-onset type 2 diabetes patients (T2D) patients before and after the treatment with rosiglitazone at 4 mg/day for 12 weeks. The rosiglitazone did not change BMI in both groups but decreased fasting glucose and HbA1c levels in the T2D group. The treatment reduced CRP, TNFa and SAA by 11-39% and increased adiponectin by 82% with statistical significance. In conclusion, we found that inflammatory adipokines were elevated in obesity and decreased in diabetics after rosiglitazone treatment, supporting that adipokines may be a mediator in the metabolic syndrome. [ABSTRACT FROM AUTHOR]

Type 2 diabetes is reported to be associated with olfactory dysfunction and cognitive decline. However, whether and how olfactory neural circuit abnormalities involve cognitive impairment in diabetes remains uncovered. This study thus aimed to investigate olfactory network alterations and the associations of odor-induced brain activity with cognitive and metabolic parameters in type 2 diabetes. Participants with normal cognition, including 51 patients with type 2 diabetes and 41 control subjects without diabetes, underwent detailed cognitive assessment, olfactory behavior tests, and odor-induced functional MRI measurements. Olfactory brain regions showing significantly different activation between the two groups were selected for functional connectivity analysis. Compared with the control subjects, patients with diabetes demonstrated significantly lower olfactory threshold score, decreased brain activation, and disrupted functional connectivity in the olfactory network. Positive associations of the disrupted functional connectivity with decreased neuropsychology test scores and reduced pancreatic function were observed in patients with diabetes. Notably, the association between pancreatic function and executive function was mediated by olfactory behavior and olfactory functional connectivity. Our results suggested the alteration of olfactory network is present before clinically measurable cognitive decrements in type 2 diabetes, bridging the gap between the central olfactory system and cognitive decline in diabetes. [ABSTRACT FROM AUTHOR]

Type 1 diabetes (T1D) is one of the major autoimmune diseases affecting children and young adults worldwide. To date, the different immunotherapies tested have achieved insulin independence in <5% of treated individuals. Recently, a novel hematopoietic stem cell (HSC)-based strategy has been tested in individuals with new-onset T1D. The aim of this study was to determine the effects of autologous nonmyeloablative HSC transplantation in 65 individuals with new-onset T1D who were enrolled in two Chinese centers and one Polish center, pooled, and followed up for 48 months. A total of 59% of individuals with T1D achieved insulin independence within the first 6 months after receiving conditioning immunosuppression therapy (with antithymocyte globulin and cyclophosphamide) and a single infusion of autologous HSCs, and 32% remained insulin independent at the last time point of their follow-up. All treated subjects showed a decrease in HbA1c levels and an increase in C-peptide levels compared with pretreat-ment. Despite a complete immune system recovery (i.e., leukocyte count) after treatment, 52% of treated individuals experienced adverse effects. Our study suggests the following: 1) that remission of T1D is possible by combining HSC transplantation and immunosuppression; 2) that autologous nonmyeloablative HSC transplantation represents an effective treatment for selected individuals with T1D; and 3) that safer HSC-based therapeutic options are required. [ABSTRACT FROM AUTHOR]

The efficacy and safety of twice daily (BID: immediately before breakfast and dinner) and thrice daily (TID: immediately before breakfast, lunch and dinner) biphasic insulin aspart 30 (BIAsp30) were assessed in this 24-week randomised, open-labeled, parallel-group trial in China. A total of 321 type 2 diabetics (FBG≥7.8mM;HbA[sub 1c]≥7.5%) inadequately controlled with oral antidiabetic agents (OADs) were randomised (1:1) to receive BID or TID BIAsp30. Subject baseline characteristics were comparable in two groups. HbA[sub 1c] were 9.5±1.4%(BID) and 9.6±.5%(TID). FBG were 11.5±2.7mM(BID) and 11.8±3. 1mM(TID). Insulin dose was adjusted to achieve pre-meal BG target of4.4-6.1mM (APDPG 2002). After 24 weeks, HbA[sub 1c] decreased significantly in both groups (BID:-2.5%;TID:-2.8%). TID group showed superiority in HbA[sub 1c] improvement (0.3%, 95% CI: [-0.53;-0.13], p<0.01). Half of subjects achieved HbA[sub 1c] target <7.0% with BIAsp30 BID. Fifteen percent more subjects reaching HbA[sub 1c]<7.0% with BIAsp30 TID. FBG in both groups showed significant reduction (BID&TID:-4.7±0.1mM). There was no significant difference in major and minor hypoglycaemic episodes between treatments, but a significant lower risk (p<0.05) for TID treatment in the subgroup of subjects achieving the target of HbA[sub 1c]< 7.0%. Risk of nocturnal events was similar in both groups (RR=0.83,p=0.60). TID group revealed significantly lower risk of overall (RR=0.62, p<0.05) and diurnal hypoglycaemic events (RR=0.58, p<0.01). The trend of significantly lower hypoglycaemic episodes was also observed in subjects achieving target of HbA[sub 1c]<7.0%. There was no significant difference for weight gain in two groups. Mean daily insulin doses were 0.82U/kg in BID group and 0.86U/kg in TID group at the end of study. In conclusion, both twice daily and thrice daily BIAsp30 were efficacious in glycaemic control in insulin naive type 2 diabetics. The regimen of thrice daily BIAsp30 could offer greater reduction in HbA[sub 1c] and lower risk of hypoglycaemic events. More patients can reach target with treatment regimen of BIASP30 TID without increasing insulin dose and weight gain compared to BID group. [ABSTRACT FROM AUTHOR]