Liver enzymes concentrations are closely related to prediabetes: findings of the Shanghai Diabetes Study II (SHDS II).

OBJECTIVE: To investigate the relationship of liver enzymes with hyperglycemia in a large population in Shanghai and identify the association between liver enzymes and insulin resistance. METHODS: A total of 3 756 participants were enrolled. Each participant underwent an oral glucose tolerance test and completed a questionnaire. Anthropometric indices were recorded and serum samples were collected for measurement. RESULTS: Liver enzymes concentrations were independently associated with i-IGT, IFG+IGT, and diabetes. With the increase of ALT and GGT concentrations, ORs for i-IGT, IFG+IGT, and diabetes increased gradually. By comparing patients in the highest quartile of GGT concentrations or ALT concentrations with those in the lowest quartile (Q1), ORs for i-IGT, IFG+IGT, or diabetes was significant after adjustment. Both ALT and GGT concentrations were linearly correlated with HOMA-IR and independently associated with HOMA-IR [ALT OR (95% CI): 2.56 (1.51-4.34) P=0.00; GGT OR (95% CI): 2.66 (1.53-4.65) P=0.00]. CONCLUSION: Serum ALT and GGT concentrations were closely related to pre-diabetes and diabetes in the Shanghai population and positively associated with insulin resistance.

Characterization of rhodamine conjugated Agiotensin II peptide: synthesis, analysis and receptor binding and internalization.

The results in this study show that the rhodamine fluorophore can be specifically conjugated to Angiotensin II at Lys3 residue (substituted for a Val) without altering the biological activity of the parent compound. The conjugated peptide was characterized using HPLC, mass spectrometry, and N-terminal sequencing. The rhodamine-Angiotensin II binds effectively to AT1 receptor and gets internalized in clathrin coated vesicles by endocytosis. These results clearly suggest the usefulness of fluorophore-conjugated peptides in studies such as, ligand-receptor binding, and ligand-receptor complex internalization, for drug delivery using cell receptors and as an alternative to peptide hormone radioimmunoassays.

Suppression of malignant growth of human breast cancer cells by ectopic expression of integrin-linked kinase.

Allelic loss at the short arm of chromosome 11 is one of the most common and potent events in the progression and metastasis of breast cancer. Here, we present evidence that the Integrin-Linked Kinase (ILK) gene maps to the commonly deleted chromosome 11p15.5 and suppresses malignant growth of human breast cancer cells both in vitro and in vivo. ILK is expressed in normal breast tissue but is downregulated in metastatic breast cancer cell lines and in advanced breast cancers. Transfection of wild-type ILK into the MDA-MB-435 mammary carcinoma cells potently suppressed their growth and invasiveness in vitro and reduced the cells' ability to induce tumors and metastasize in athymic nude mice. Conversely, expression of the ankyrin repeat or catalytic domain mutants of ILK failed to suppress the growth of these cells. Growth suppression by ILK is not due to apoptosis but is mediated by its ability to block cell-cycle progression in the G1 phase and by modulating the levels of integrins. These findings directly demonstrate that ILK deficiency facilitates neoplastic growth and invasion and suggest a novel role for the ILK gene in the suppression of tumor metastasis.