Type 2 diabetes is a high-profile global public health problem, particularly in Asia. The young age of onset, low body mass index, and early appearance of pancreatic islet dysfunction are characteristics of Asian patients with T2DM. Metabolic surgery has become the standard treatment for T2DM patients and can significantly improve T2DM through a variety of mechanisms including modulation of energy homeostasis and reduction of body fat mass. Indeed, restoration of islet function also plays an integral role in the remission of T2DM. After metabolic surgery, islet function in Asian T2DM patients has improved significantly, with proven short-term and long-term effects. In addition, islet function is an important criterion and reference for patient selection prior to metabolic surgery. The mechanism of islet function improvement after metabolic surgery is not clear, but postoperative anatomical changes in the gastrointestinal tract leading to a number of hormonal changes seem to be the potential cause, including glucagon-like peptide-1, gastric inhibitory polypeptide, peptide YY, ghrelin, and cholecystokinin. The authors analyzed the current retrospective and prospective studies on the effect of metabolic surgery on the islet function of Asian T2DM patients with a low BMI and its mechanism, summarized the clinical evidence that metabolic surgery improved islet function in Asian T2DM patients with a low BMI, and discussed its underlying mechanism. It is of great significance for realizing personalized and precise treatment of metabolic surgery and further improving its clinical benefits.
Bariatric Surgery ; Body Mass Index ; Cholecystokinin/therapeutic use* ; Diabetes Mellitus, Type 2/surgery* ; Gastric Inhibitory Polypeptide/therapeutic use* ; Ghrelin/therapeutic use* ; Glucagon-Like Peptide 1/therapeutic use* ; Humans ; Peptide YY/therapeutic use* ; Prospective Studies ; Retrospective Studies ; Treatment Outcome

OBJECTIVETo investigate the therapeutic effects of peptide YY against hepatic fibrosis in rats and explore the possible mechanism.

METHODRat models of hepatic fibrosis were established with a subcutaneous injection of carbon tetrachloride and randomized into normal control group, model group, peptide YY (PYY)-treated group, octreotide-treated group, and interferon gamma-treated group. Serum levels of the hepatic function indices and hepatic fibrotic index were detected, and the hepatic fibrosis grade was assessed using HE staining. The expression of transforming growth factor beta1 (TGFbeta1) were determined with immunohistochemical staining method.

RESULTSThe rats in PYY-treated group showed significantly different serum levels of TBIL, HA and LN from the rats in the model group (P<0.05). PYY significantly reduced hepatic fibrosis scores and lowered TGFbeta1 expression as compared with the model group.

CONCLUSIONSPYY can down-regulate TGFbeta1 expression to inhibit the development of hepatic fibrosis with comparable efficacy with interferon gamma and octreotide.

Animals ; Carbon Tetrachloride ; Immunohistochemistry ; Liver Cirrhosis, Experimental ; chemically induced ; drug therapy ; metabolism ; Male ; Peptide YY ; therapeutic use ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Transforming Growth Factor beta1 ; biosynthesis

OBJECTIVETo investigate the effects of peptide YY (PYY) on subcutaneous transplantation tumor of human hepatoma in nude mice and preliminarily explore the mechanisms.

METHODSHepG2 human hepatic carcinoma cells were injected into nude mice subcutaneously, and the resultant tumor were taken and prepared into small tissue blocks. The tissue blocks were implanted subcutaneously into nude mice to establish mouse models bearing human hepatoma. Thirty-two such mouse models were assigned equally into 4 groups to receive subcutaneous PYY injection at a high or low dose, intraperitoneal injection of floxuridine (positive control group), or subcutaneous normal saline injection (negative control group). The general condition of the tumor-bearing mice and the growth of the tumors were observed.

RESULTSCompared with the negative control group, the high- and low-dose PYY groups showed reduced gross tumor volume, lowered serum AFP, tumor weight, and cAMP content in the tumor tissue (P<0.05).

CONCLUSIONPYY can inhibit the growth of subcutaneous hepatoma in nude mice, which might be associated with the reduction of cAMP content in the tumors following PYY treatment.

Animals ; Carcinoma, Hepatocellular ; drug therapy ; pathology ; Cell Line, Tumor ; Cyclic AMP ; metabolism ; Humans ; Liver Neoplasms, Experimental ; drug therapy ; metabolism ; pathology ; Male ; Mice ; Mice, Inbred BALB C ; Mice, Nude ; Peptide YY ; therapeutic use ; Tumor Burden ; drug effects ; Xenograft Model Antitumor Assays