Metabolic and Functional Specializations of Pancreatic Beta Cell
A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Endocrinology and Metabolism".
Deadline for manuscript submissions: closed (31 December 2023) | Viewed by 4691
Special Issue Editor
Interests: diabetes; biphasic kinetic of insulin secretion; glucose homeostasis; insulin secretion; pancreas islet beta cell; glucose
Special Issue Information
Dear Colleagues,
Despite intensive research activities in the area of stimulus–secretion coupling in the pancreatic beta-cell, many open questions remain. One may even feel that with the increased amount of data available, the number of controversial issues has increased, e.g., it has been questioned whether the rise of the ATP/ADP ratio in cytosol during glucose stimulation really results from the increased activity of the oxidative phosphorylation. In addition, it has been argued that cataplerosis, which is apparently intimately linked to the stimulus–secretion coupling of the beta-cell, does not involve the export of citrate, which was originally believed to be firmly established. Apparently, the function of the beta-cell mitochondria is more complex and less well-understood than current textbook knowledge suggests.
For the present Special Issue of IJMS, manuscripts exploring the mitochondrial metabolism during the physiological and pathophysiological regulation of insulin secretion, with an emphasis on processes specific to the beta-cell, are invited. In other words, what sets the beta-cell apart from other endocrine islet cells? Specifically, topics of interest include, but are not restricted to, the following:
- The tight coupling of glycolysis to the mitochondrial metabolism: how important are the glycerophosphate and malate–aspartate shuttle systems?
- Pyruvate-dehydrogenase and -carboxylase gene expression and activity: why does the beta cell need pyruvate carboxylase?
- GABA synthesis in the beta cell: are the GABA shunt and its enzymes (glutamic acid decarboxylase = GAD65, GABA transaminase, and semialdehyde succinic acid dehydrogenase) only needed to exert paracrine inhibition?
- Is GABA shunt metabolism conditioning mitochondrial ATP production via the glucose metabolism in the citric acid cycle?
- Mitochondrial signaling to exocytosis beyond the ATP/ADP ratio: it exists, but through which signals and which mechanisms?
- Mitochondrial structure: how important are fusion/fission and mitophagy for beta-cell signal transduction?
- The role of fatty acids in the beta-cell: when is the beta-oxidation active and what are the consequences?
The editors believe that these very basic topics can be addressed in insulin-secreting cell lines as well as in primary beta cells and islets from rodents and humans.
Prof. Dr. Ingo Rustenbeck
Guest Editor
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Keywords
- diabetes
- pancreatic β-cells
- tumoral β-cells
- insulin secretion
- pyruvate-dehydrogenase
- pyruvate-carboxylase
- cataplerosis
- GABA shunt
- mitochondrial metabolism
- β-cell models
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