Anat Cell Biol.  2015 Mar;48(1):16-24. 10.5115/acb.2015.48.1.16.

Mechanistic insights into pancreatic beta-cell mass regulation by glucose and free fatty acids

Affiliations
  • 1Lee Gil Ya Cancer and Diabetes Institute, Gachon University, Incheon, Korea. with62@gachon.ac.kr
  • 2Gachon Medical Research Institute, Gil Hospital, Incheon, Korea.

Abstract

Pancreatic islets are responsible for blood glucose homeostasis. Reduced numbers of functional (insulin-secreting) beta-cells in pancreatic islets underlies diabetes. Restoration of the secretion of the proper amount of insulin is a goal. Beta-cell mass is increased by neogenesis, proliferation and cell hypertrophy, and is decreased by beta-cell death primarily through apoptosis. Many hormones and nutrients affect beta-cell mass, and glucose and free fatty acid are thought to be the most important determinants of beta-cell equilibrium. A number of molecular pathways have been implicated in beta-cell mass regulation and have been studied. This review will focus on the role of the principle metabolites, glucose and free fatty acid, and the downstream signaling pathways regulating beta-cell mass by these metabolites.

Keyword

Glucose; Free fatty acids; Beta-cell mass regulation; Proliferation; Apoptosis

MeSH Terms

Apoptosis
Blood Glucose
Fatty Acids, Nonesterified*
Glucose*
Homeostasis
Hypertrophy
Insulin
Islets of Langerhans
Blood Glucose
Fatty Acids, Nonesterified
Glucose
Insulin

Figure

  • Fig. 1 Beta-cell mass regulation in db/db mice. Images of islet morphology at 4, 12, and 24 weeks of age in db/db mice. Sections were immunohistochemically stained for insulin and glucagon as a measurement of beta-cells (green) and alpha-cells (red). Scale bars=20 µm.


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