Relationship between serum cystatin C and serum adiponectin level in type 2 diabetic patients.

Background: To investigate the relationship between serum levels of cystatin C and adiponectin in patients with type 2 diabetes.

Methods: We examined serum cystatin C and adiponectin levels in 234 patients with type 2 diabetes who visited our hospital.

Results: The serum level of cystatin C was positively correlated with age (P < 0.

Long-term suppressive effect of octreotide on progression of metastatic gastrinoma with multiple endocrine neoplasia type 1: seven-year follow up.

A 30-year-old woman had a history of prolactinoma and primary hyperparathyroidism. She was diagnosed as having multiple endocrine neoplasia type 1 with gastrinoma and liver metastases. Octreotide therapy was started and the serum gastrin level decreased immediately.

Thyroid follicular adenoma producing parathyroid hormone-related protein with a normal serum calcium level.

A 64-year-old woman had normal serum calcium and plasma parathyroid hormone levels, despite an extremely high plasma parathyroid hormone-related protein (PTHrP) level. She underwent medical screening at our hospital and several neck tumors were detected by ultrasonography. After surgical resection of these tumors, her plasma PTHrP level was normalized.

Functional characterization of the HNF4alpha isoform (HNF4alpha8) expressed in pancreatic beta-cells.

Mutations in the hepatocyte nuclear factor (HNF) 4alpha gene cause a form of maturity-onset diabetes of the young (MODY1), which is a monogenic form of type 2 diabetes characterized by impaired insulin secretion by pancreatic beta-cells. HNF4alpha is a transcription factor expressed in the liver, kidney, intestine, and pancreatic islet. Multiple splice variants of the HNF4alpha gene have been identified and an isoform of HNF4alpha8, an N-terminal splice variant, is expressed in pancreatic beta-cells.

Thyroid hormone receptor interacting protein 3 (trip3) is a novel coactivator of hepatocyte nuclear factor-4alpha.

Mutations of the hepatocyte nuclear factor-4alpha (HNF-4alpha) gene are associated with a subtype of maturity-onset diabetes of the young (MODY1) that is characterized by impaired insulin secretion in response to a glucose load. HNF-4alpha, which is a transcription factor expressed in pancreatic beta-cells, plays an important role in regulating the expression of genes involved in glucose metabolism. Thus, cofactors that interact with HNF-4alpha and modify its transcriptional activity might also play an important role in regulating the metabolic pathways in pancreatic beta-cells, and the genes of such cofactors are plausible candidate genes for MODY.

Overexpression of dominant-negative mutant hepatocyte nuclear fctor-1 alpha in pancreatic beta-cells causes abnormal islet architecture with decreased expression of E-cadherin, reduced beta-cell proliferation, and diabetes.

One subtype of maturity-onset diabetes of the young (MODY)-3 results from mutations in the gene encoding hepatocyte nuclear factor (HNF)-1 alpha. We generated transgenic mice expressing a naturally occurring dominant-negative form of human HNF-1 alpha (P291fsinsC) in pancreatic beta-cells. A progressive hyperglycemia with age was seen in these transgenic mice, and the mice developed diabetes with impaired glucose-stimulated insulin secretion.