An important property of stem cells is their ability to self-renew and to differentiate into multi-lineage cells. Stem cells have been shown to differentiate into many cell types, such as insulin-secreting cells and vascular endothelial cells, and therefore offer the promise of a new regenerative medicine in the treatment of diabetes and its complications. The issues and progress involved in the stem cell therapy of diabetes are briefly commented in this article.

Early intervention and preservation of β-cell function are essential for optimal glycemic control in the long term.Available data support the early use of the long-acting glucagon-like peptide-1 analogue liraglutide in preservation of β-cell mass and function,leading to better glycemic control.Besides glycemic control,persistent weight loss and reduced visceral adiposity are observed in type 2 diabetic patients treated with liraglutide,linking to its potential cardio-protective effects.

The aim of translational medicine is to transform currently available knowledge into useful measures for daily clinical practice.Translational medical research needs to incorporate the resources and ways of studying complex healthcare systems.Therefore,the challenges and opportunities offered by translational medical research are tremendous.This review discusses the advance of translational medical research,especially the case of endocrinoloical and metabolic disease.

An important property of stem cells is their ability to self-renew and to differentiate into multi-lineage cells. Stem cells have been shown to differentiate into many cell types, such as insulin-secreting cells and vascular endothelial cells, and therefore offer the promise of a new regenerative medicine in the treatment of diabetes and its complications. The issues and progress involved in the stem cell therapy of diabetes are briefly commented in this article.

Action for Health in Diabetes( Look AHEAD) trial showed that an intensive lifestyle intervention focusing on weight loss did not reduce the rate of cardiovascular events in overweight or obese adult patients with type 2 diabetes. However, the intensive lifestyle intervention improved the control levels of the risk factors for cardiovascular disease, attenuated the obesity-associated comorbidities, and improved the quality of life in these patients.

Stem cells with the capacity of self-renewal and multilineage differentiation are promising sources for generation of pancreatic cells for cell replacement therapy in diabetes mellitus.Stem cells also show their potential in the studies regarding the embryonic development of several endocrine organs including pancreatic islets,thyroid,parathyroid,and adrenal glands.Moreover,they would be much useful for investigation of pathogenesis and drug screening in endocrine and metabolic diseases.

In post-trial follow-up of DCCT,UKPDS and Steno-2 studies,sustained beneficial effects on the risk reductions for microvascular and macrovascular complications has been observed in previous intensive treatment group,suggesting that patients with diabetes benefit mostly from early intensive blood glucose control.On the other hand,intensive glucose lowering therapy has been shown to increase the risk of all cause mortality in high-risk patients with type 2 diabetes in ACCORD study.Therefore,the target of blood glucose control should be individualized for each diabetic patient.Not only intensive glucose lowering therapy but also avoidance of hypoglycemia during therapy should be highly considered.

Objective To investigate if there is any effect of interleukin-18 (IL-18) or if IL-18 modulates IL-1? effects on islet function.Methods Insulin release and nitrite production from isolated islets of newborn Wistar rats were measured after incubation with or without cytokines.Reverse transcription polymerase chain reaction (RT-PCR) was used to detect mRNA expression of the IL-18 receptor signaling chain (IL-18R?).Results (1) There were no significant effects of 0.625～10nmol/L of recombinant murine (rm) IL-18 alone on accumulated or glucose-challenged insulin release and nitrite production after 24h.(2) 15pg/ml of recombinant human (rh) IL-1? significantly increased nitrite production and inhibited insulin release.However,0.625～10nmol/L of rm IL-18 failed to modulate the above effects caused by IL-1?.(3) 24h rm IL-12 preincubation failed to sensitize islets to the effects of 10nmol/L of rm or recombinant rat (rr) IL-18 alone or to prime islets to IL-1? actions on insulin release and nitrite production.(4) IL-18R? mRNA was not expressed in isolated islets even after exposure to IL-12 for 48h.Conclusion Unlike IL-1?,IL-18 dose not play a direct role in the destruction of islet ?-cell function.

Metformin improves glycemic control mainly due to improved insulin sensitivity.Dipeptidyl peptidase-4(DPP-4) inhibitor,which suppresses degradation of glucagon-like peptide-1 (GLP-1) and maintains the bioactivity of endogenous GLP-1,improves islet dysfunction.Moreover,recent studies suggested that metformin enhanced the biological effect of GLP-1 via different mechanisms and that DPP-4 inhibitor enhanced insulin sensitivity in type 2 diabetes.Therefore,the combination therapy of DPP-4 inhibitor and metformin could simultaneously ameliorate the two major defects of type 2 diabetes and obtain complementary and synergistic benefits for glycemic control.

Objective　To investigate if there is any effect of interleukin-18 (IL-18) or if IL-18 modulates IL-1β effects on islet fun ction.Methods　Insulin release and nitrite production from isolated islets of newborn Wistar rats were measured after incubation with or w ithout cytokines.Reverse transcription polymerase chain reaction (RT-PCR) was u sed to detect mRNA expression of the IL-18 receptor signaling chain (IL-18Rβ) .Results　(1) There were no significant effects of 0.625～ 10nmol/L of recombinant murine (rm) IL-18 alone on accumulated or glucose-cha llenged insulin release and nitrite production after 24h.(2) 15pg/ml of recombi nant human (rh) IL-1β significantly increased nitrite production and inhibited insulin release.However,0.625～10nmol/L of rm IL-18 failed to modulate the abo ve effects caused by IL-1β.(3) 24h rm IL-12 preincubation failed to sensitize islets to the effects of 10nmol/L of rm or recombinant rat (rr) IL-18 alone or to pri me islets to IL-1β actions on insulin release and nitrite production.(4) IL-1 8Rβ mRNA was not expressed in isolated islets even after exposure to IL-12 for 48h.Conclusion　Unlike IL-1β,IL-18 dose not play a dir ect role in the destruction of islet β-cell function.