The role of G-protein-coupled receptor kinase 2 in diabetic mechanical hyperalgesia in rats.

Background: Previous studies have indicated a negative correlation between GRK2 expression and pain development and transmission. Here, we investigated whether G-protein-coupled receptor kinase 2 (GRK2) was involved in regulating diabetic mechanical hyperalgesia (DMH).

Methods: The adeno-associated viral vectors containing the GRK2 gene (AAV-GRK2) were used to up-regulate GRK2 protein expression.

Sequence of fat partitioning and its relationship with whole body insulin resistance.

Background: Currently it is unclear whether lipid accumulation occurs in a particular sequence and its relationship with whole body insulin resistance (IR). This study aimed to answer this question.

Methods: Male Sprague-Dawley (SD) rats were fed on a normal or a high-fat diet for 20 weeks.

Role and mechanism of uncoupling protein 2 on the fatty acid-induced dysfunction of pancreatic alpha cells in vitro.

Background: Uncoupling protein (UCP) 2 is related to the dysfunction of beta cells induced by fatty acids. However, whether UCP2 has similar effects on alpha cell is still not clear. This study aimed to investigate the effects of UCP2 and its possible mechanisms in lipotoxicity-induced dysfunction of pancreatic alpha cells.

[Relationship between oxidative stress and beta cell lipoapoptosis in rats].

Objective: To investigate the effect of beta cell lipoapoptosis after long term high-fat feeding in rats, and to investigate the relationship between oxidative stress, gene expression and beta cell lipoapoptosis.

Methods: Forty-one SD male rats were randomly divided into 2 groups: high-fat diet group (HF group) and control group (NC group). At the end of 28 weeks, the levels of malondialdehyde (MDA) and glutamylcysteinylglycine (GSH) in plasma and pancreatic tissue,the early-phase insulin secretion in beta cells, the beta cell apoptosis (TUNEL technology) and the uncoupling protein 2 (UCP2) gene expression in islets were measured.

[Relationship between islet beta cell dysfunction and gene expression of uncoupling protein-2 and possible mechanism thereof].

Objective: To study the effects of high fat diet on the functions of islet beta cells and the role of uncoupling protein-2 (UCP2) therein and possible mechanism.

Methods: Forty SD rats were randomly divided into two equal groups: high-fat-(HF) diet group, fed with HF diet for 20 weeks, and normal diet control (NC) group, fed with normal diet. At the end of the twentieth week blood samples were collected from the heart to determine the serum fasting blood glucose (FBG) and fasting insulin (FINS), and plasma nitrotyrosine, malondialdehyde (MDA), and glutamylcysteinylglycine (GSH), indicators of oxidative stress.

[Effects of fenofibrate on gene expression of carnitine palmitoyltransferase 1 in liver and skeletal muscle and its influence on insulin sensitivity].

Objective: To study the effects of fenofibrate (FF), a peroxisome proliferator activated receptor (PPAR) alpha activator, on the expression of carnitine palmitoyltransferase 1 (CPT-1) mRNA in liver and muscle and its influence on insulin sensitivity.

Methods: Thirty-two normal 8 week-old male SD rats were randomly divided into 3 groups: normal control group, fed with normal food for 3 weeks (NC group, n = 10), high fat diet group, fed with high fat food (HF group, n = 10), and high fat diet supplemented with FF group, fed with high fat food and given with gastric perfusion of FF (50 mg x kg(-1) x d(-1)) (FF group, n = 12). Fast serum triglyceride (TG) level was tested by automatic biochemical analyzer after 8-10 h fasting.

[The mechanism of and relationship between lipid metabolism genes expression and insulin resistance in high fat-fed mice].

Objective: To observe the relationship between changes of genes expression related to lipid metabolism and insulin resistance induced by high fat diet in SD rats.

Methods: Normal 8-week old male SD rats were randomly divided into 3 groups. They were fed with normal chow (NC, n = 10), high fat diet (HF, n = 10) and high fat diet supplemented with pioglitazone 15 mg x kg(-1) x d(-1) (HP, n = 12).

[The relationship between islet alpha cell insulin resistance and inflammatory pathway activation and its mechanism].

Objective: To study the changes of inflammatory path molecules in the islet alpha cells in high-fat-diet fed plus beta cell-deleted rat models and the effects of pioglitazone intervention.

Methods: Forty five normal male SD rats, 8 week old, were randomly divided into 3 groups, i.e.

[Effect of lipid infusion on the function of islet beta cells and gene expression of insulin signal transduction system].

Objective: To study the changes and mechanism of the function of islet beta cells and insulin signal transduction molecules after lipid infusion.

Methods: Twenty five SD rats were randomly divided into 2 groups, FFA group and NS group. Catheters were implanted under pentobarbital anesthesia in the right atrium via the jugular vein and the left carotid artery.

[The expression of insulin signal transduction molecules and islet alpha cell insulin resistance].

Objective: To study the changes of insulin signal transduction molecules in islet alpha cells in high-fat-diet plus beta cell-deleting rat models and its underlying mechanism.

Methods: Thirty SD rats were randomly divided into 2 equal groups and fed with high-fat-diet (HF group) or normal diet (normal control group, NC group) respectively. At the end of twenty-week feeding, the fasting serum insulin (Ins), glucagon (Glc), free fatty acid (FFA), and triglyceride (TG were measured.