Lens is a perfect optical organ,which roots in the surface ectoblast and has good quality of light penetration and refraction.It consists of lens bursa,epithelia,cortex and nucleus from exterior to interior in turn.The life center of lens is the epithelia which not only excretes collagen Ⅳ to form lens bursa outside,and gradually develops to fiber cell to form cortex and nucleus of lens,but also supports all the energy of lens metabolism.Aldose reductase can be activated by high glucose in a long time.Then,the sorbitol accumulation of lens epithelial cells and fibre cells causes cortex to absorb water and expand.Besides,some research results showed that p-glyprotein,clcn3(Cl-channel 3) and aquaporin were also involved in the high osmotic expansion of the lens.

Insulin resistance ,a key component of type 2 diabetes,is recognized as the pathological basis of the metabolic syndrome. H owever,its underlying mechanisms are still not fully understood.Recently,eleva ted levels of free fatty acids (FFA)have been observed in many insulin-resist ance states,which has gradually drawn attention.Not only do FFA interfere in se veral steps involved in glucose metabolism,but also play an important role in i nsulin signal transduction,resulting in decreased insulin-stimulated glucose t ransport. The thiazolidinediones,as insulin-sensitizing drugs,have entered th e market. A prominent effect of these agents is the lowering of circulating FFA levels and it is believed that targeting FFA metabolism may therefore offer wide r expectations in therapy for insulin resistance and type 2 diabetes.

With the development of proteomics, the application in the research for the function of proteins becomes popular. This review article presents that proteomics, a kind of tools of molecular biology, has been successfully used for studying the pathogenesis of type 1 and type 2 diabetes.

Glucokinase (GK) is considered to be the key regulatory enzyme in glucose metabolism, whose activity changing will lead to glucose metabolic disturbance and diabetes. Recently, people have realized that there is a good extensive perspective in diabetes research by means of glucokinase investigation. In this paper, we review the mechanism of diabetes resulting from abnormality of glucokinase activity and the status of glucokinase activators, propose the viewpoint that glucokinase is a powerful target for diabetes therapy and research, and illuminate that searching of glucokinase activators is the guidance in the future.

Aim To study the effect of gelatinized starch on starch tolerance test.Methods Acarbose with gelatinized starch or ungelatinized starch was administered to ICR mice by gavage,and blood samples were collected at 30,60 and 120 minutes after treatment to measure blood glucose levels,whose rising percentage calculated at 30 min and AUC in every group.Results Compared with the ungelatinizedstarch group,blood glucose levels at 30 and 60 minutes after starch loading were significantly elevated in the gelatinized-starch group.Acarbose drastically flatted the elevation of blood glucose after gelatinized-starch load,but it had little effect on the ungelatinized-starch test.Conclusion It is more feasible to use gelatinized starch to carry out starch tolerance test than to use ungelatinized starch.

PPAR? is a kind of nuclear receptors responsible for the regulation of glucose and lipid metabolisim and adipocyte difference,which is related with the pathogenesis of obesity,insulin resistance and type 2 diabetes mellitus.PPAR? agonists as insulin sensitizer have been used in the clinical treatment for type 2 diabetes for more than decades.Recently,with the further research plunging into the PPAR signaling pathway and insulin sensitizer,the recognition of this crucial nuclear receptor has been renewed and developed.The aim of this review is to report the update research outcomes.

AIM　To study the glucose and lipids metabolis m and insulin sensitivity of MSG rats during their growing period, and to evalua te the effects of insulin sensitizer pioglitazone on the model rats. MET HODS　Body weights were measured regularly, and glucose and insulin tole rance tests were taken. In their 3 and 10 months old, rats were given insulin se nsitizer pioglitazone orally, then the effects on serum glucose, triglyceride, c holesteral, free fatty acid and insulin concentrations were determined. RESULTS　Compared with normal rats, a slight but significant increase of glucose in MSG rats was revealed. The serum triglyceride, cholesteral, free fat ty acid and insulin concentrations were significantly higher in model rats. More over, gluconeogenesis increased significantly, and insulin tolerance showed abno rmal. However, glucose tolerance was nearlly normal. Pioglitazone could ameliora te all these metabolic disorders. CONCLUSION　Obesity and insuli n resistance were induced by injecting monosodium glutamate (MSG) to neonatal Wi star rats. Pioglitazone can significantly improve the insulin sensitivity of MSG rats. These results suggested that MSG obese rats can be used as an easily acce ssible and inexpensive insulin resistance animal model for evaluating the effica cy and mechanisms of antidiabetic agents.

Peroxisome proliferator activated receptor(PPAR), a member of the hormone receptor superfamily, is a key regulating factor in adipocyte differentiation and lipids metabolism. Recently, with the increased understanding of the precise mechanisms of TZD, thiazolidinedione class of insulin sensitizer, PPAR? has also been identified as the major functional receptor for the drugs. In the study of the relationship between PPAR and insulin resistance, considerable gaps appeared. TZD induced activation of PPAR? is known to promote insulin sensitivity. More interestingly, however, PPAR? +/- heterozygous mice were shown to be less susceptible to insulin resistance. These findings suggest that the relationship between PPAR activation and insulin sensitivity improvement is not simplely positively related. A better understanding of the role of PPAR in insulin action system will be critical in developing more efficacious and safe agents that act on PPAR and benefit patients with type 2 diabetes.

This study aims to establish a method to determine the serum acetaminophen concentration based on diazo reaction, and apply it in the gastric emptying evaluation. Theoretically, acetaminophen could take hydrolysis reaction in hydrochloric acid solution to produce p-aminophenol, which could then take diazo reaction resulting in a product with special absorption peak at 312 nm. Then the serum acetaminophen concentration and recovery rate were calculated according to the standard curve drawn with absorbance at 312 nm. ICR mice were given a dose of acetaminophen (500 mg x kg(-1)) by gavage and the serum acetaminophen was dynamically measured through the diazo reaction. Besides, ICR mice were subcutaneously injected with the long-acting GLP-1 analog GW002 before the gavage of acetaminophen, and serum acetaminophen concentration was measured as above to study how GW002 could influence the gastric emptying. The data showed acetaminophen ranging from 0 to 160 μg x mL(-1) could take diazo reaction with excellent linear relationship, and the regression equation was y = 0.0181 x +0.0104, R2 = 0.9997. The serum acetaminophen was also measured with good linear relationship (y = 0.0045 x + 0.0462, R = 0.9982) and the recovery rate was 97.4%-116.7%. The serum concentration of acetaminophen reached peak at about 0.5 h after gavage, and then gradually decreased. GW002 could significantly lower the serum acetaminophen concentration and make the area under the concentration-time curve (AUC) decrease by 28.4%. In conclusion, a method for the determination of serum acetaminophen based on the diazo reaction was established with good accuracy and could be used in the evaluation of gastric emptying.