Imeglimin mitigates the accumulation of dysfunctional mitochondria to restore insulin secretion and suppress apoptosis of pancreatic β-cells from db/db mice.

Mitochondrial dysfunction in pancreatic β-cells leads to impaired glucose-stimulated insulin secretion (GSIS) and type 2 diabetes (T2D), highlighting the importance of autophagic elimination of dysfunctional mitochondria (mitophagy) in mitochondrial quality control (mQC). Imeglimin, a new oral anti-diabetic drug that improves hyperglycemia and GSIS, may enhance mitochondrial activity. However, chronic imeglimin treatment's effects on mQC in diabetic β-cells are unknown.

A new beta cell-specific mitophagy reporter mouse shows that metabolic stress leads to accumulation of dysfunctional mitochondria despite increased mitophagy.

Aims/hypothesis: Mitophagy, the selective autophagy of mitochondria, is essential for maintenance of mitochondrial function. Recent studies suggested that defective mitophagy in beta cells caused diabetes. However, because of technical difficulties, the development of a convenient and reliable method to evaluate mitophagy in beta cells in vivo is needed.

ELKS/Voltage-Dependent Ca Channel-β Subunit Module Regulates Polarized Ca Influx in Pancreatic β Cells.

Pancreatic β cells secrete insulin by Ca-triggered exocytosis. However, there is no apparent secretory site similar to the neuronal active zones, and the cellular and molecular localization mechanism underlying polarized exocytosis remains elusive. Here, we report that ELKS, a vertebrate active zone protein, is used in β cells to regulate Ca influx for insulin secretion.

VAMP7 Regulates Autophagosome Formation by Supporting Atg9a Functions in Pancreatic β-Cells From Male Mice.

Dysfunctional mitochondria are observed in β-cells of diabetic patients, which are eventually removed by autophagy. Vesicle-associated membrane protein (VAMP)7, a vesicular SNARE protein, regulates autophagosome formation to maintain mitochondrial homeostasis and control insulin secretion in pancreatic β-cells. However, its molecular mechanism is largely unknown.

Alterations in emotional responses (pleasantness/unpleasantness) induced by sniffing food odors during chemotherapy in patients with lung cancer.

Background: Patients receiving chemotherapy experience anorexia and food aversion in their daily lives, and one of the causes is the smell of food. However, it is not clear why the aversion to these smells occurs. This study aimed to determine the emotional responses of patients when they sniff representative food odors during chemotherapy and to investigate factors influencing smell-induced food aversion.