Exercise and inactivity as modifiers of β cell function and type 2 diabetes risk.
Liam G HallJohn P ThyfaultJames D JohnsonPublished in: Journal of applied physiology (Bethesda, Md. : 1985) (2023)
Exercise and regular physical activity are beneficial for the prevention and management of metabolic diseases such as obesity and type 2 diabetes, whereas exercise cessation, defined as deconditioning from regular exercise or physical activity that has lasted for a period of months to years, can lead to metabolic derangements that drive disease. Adaptations to the insulin-secreting pancreatic β-cells are an important benefit of exercise, whereas less is known about how exercise cessation affects these cells. Our aim is to review the impact that exercise and exercise cessation have on β-cell function, with a focus on the evidence from studies examining glucose-stimulated insulin secretion (GSIS) using gold-standard techniques. Potential mechanisms by which the β-cell adapts to exercise, including exerkine and incretin signaling, autonomic nervous system signaling, and changes in insulin clearance, will also be explored. We will highlight areas for future research.
Keyphrases
- physical activity
- high intensity
- type diabetes
- resistance training
- induced apoptosis
- body mass index
- metabolic syndrome
- stem cells
- cardiovascular disease
- blood pressure
- cell cycle arrest
- single cell
- risk assessment
- adipose tissue
- weight gain
- body composition
- signaling pathway
- cell death
- endoplasmic reticulum stress
- skeletal muscle
- pi k akt
- case control