Deteriorated high-fat diet-induced diabetes caused by pancreatic β-cell-specific overexpression of Reg3β gene in mice.

Reg family proteins have long been implicated in islet β-cell proliferation, survival, and regeneration. In our previous study, we reported that Reg3β overexpression did not increase islet growth but prevented streptozotocin-induced islet damage by inducing specific genes. In order to explore its role in type 2 diabetes (T2D), we established high-fat diet (HFD)-induced obesity and diabetes in RIP-I/Reg3β mice.

The expression of dominant negative TCF7L2 in pancreatic beta cells during the embryonic stage causes impaired glucose homeostasis.

Objective: Disruption of TCF7L2 in mouse pancreatic β-cells has generated different outcomes in several investigations. Here we aim to clarify role of β-cell TCF7L2 and Wnt signaling using a functional-knockdown approach.

Methods: Adenovirus-mediated dominant negative TCF7L2 (TCF7L2DN) expression was conducted in Ins-1 cells.

GLP-1(28-36) improves β-cell mass and glucose disposal in streptozotocin-induced diabetic mice and activates cAMP/PKA/β-catenin signaling in β-cells in vitro.

Recent studies have demonstrated that the COOH-terminal fragment of the incretin hormone glucagon-like peptide-1 (GLP-1), a nonapeptide GLP-1(28-36)amide, attenuates diabetes and hepatic steatosis in diet-induced obese mice. However, the effect of this nonapeptide in pancreatic β-cells remains largely unknown. Here, we show that in a streptozotocin-induced mouse diabetes model, GLP-1(28-36)amide improved glucose disposal and increased pancreatic β-cell mass and β-cell proliferation.

New insight into the mechanisms underlying the function of the incretin hormone glucagon-like peptide-1 in pancreatic β-cells: the involvement of the Wnt signaling pathway effector β-catenin.

During the past two decades, the exploration of function of two incretin hormones, namely glucagon-like peptide-1 (GLP-1) and gastric inhibitory peptide (GIP), has led to the development of two categories of novel therapeutic agents for diabetes and its complications, known as GLP-1 receptor (GLP-1R) agonists and DPP-IV inhibitors. Mechanisms underlying the function of GLP-1, however, still need to be further explored. GLP-1 not only functions as an incretin hormone in stimulating insulin secretion in response to nutritional, hormonal and neuronal stimulations, but also acts as an "insulin-like" factor in β-cell and extra-pancreatic organs.

Coordinated age-dependent and pancreatic-specific expression of mouse Reg2Reg3α, and Reg3β genes.

Reg family proteins such as Reg1 and islet neogenesis-associated protein (INGAP) have long been implicated in the growth and/or neogenesis of pancreatic islet cells. Recent reports further suggest similar roles to be played by new members such as Reg2, Reg3α, and Reg3β. We have studied their age-, isoform-, and tissue-specific expressions.

Pancreatic islet-specific overexpression of Reg3β protein induced the expression of pro-islet genes and protected the mice against streptozotocin-induced diabetes mellitus.

Reg family proteins have been implicated in islet β-cell proliferation, survival, and regeneration. The expression of Reg3β (pancreatitis-associated protein) is highly induced in experimental diabetes and acute pancreatitis, but its precise role has not been established. Through knockout studies, this protein was shown to be mitogenic, antiapoptotic, and anti-inflammatory in the liver and pancreatic acinars.

[Association of L-selectin gene polymorphism with susceptibility to coronary heart disease].

Objective: To investigate the possible association between L-selectin gene P213S polymorphism and coronary heart disease (CHD) in Chinese population.

Methods: In total 212 CHD patients diagnosed by angiography and 230 healthy controls were studied. The genotype and allele frequencies of L-selectin gene polymorphism were assayed by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP).

[Association of C-159T polymorphism in promoter region of CD14 and coronary heart disease].

Objective: To investigate the distribution of CD14 promoter gene -159(C>T) polymorphism in Hubei Han population of China and analyze the association of CD14 polymorphisms with coronary heart disease (CHD).

Methods: Genotypes of CD14 were typed in 162 CHD patients and 196 controls by polymerase chain reaction-restriction fragment length polymorphism. Selected coronary angiography was performed in 162 CHD patients.