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At the turn of the 19th century, Ivan Pavlov and others established that the secretion of pancreatic juice is induced upon entry of acidic chyme into the duodenum, and that this pancreatic secretion is accelerated by infusion of hydrochloric acid (HCL) into the stomach. Pavlov hypothesized that secretion of pancreatic juice is induced via a neuronal reflex; however, pancreatic secretion prevailed in dogs following denervation of the intestinal vagal and splanchnic nerves, indicating that pancreatic secretion must be mediated by another, as yet unknown, mechanism.

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Physical training reduces cell senescence and associated insulin resistance in skeletal muscle

Agnieszka Podraza-Farhanieh, Rosa Spinelli, Federica Zatterale, Annika Nerstedt, ... Ulf Smith

Physical training reduces cell senescence and associated insulin resistance in skeletal muscle

Background

Cell senescence (CS) is a key aging process that leads to irreversible cell cycle arrest and an altered secretory phenotype. In skeletal muscle (SkM), the accumulation of senescent cells contributes to sarcopenia. Despite exercise being a known intervention for maintaining SkM function and metabolic health, its effects on CS remain poorly understood.

Objectives

This study aimed to investigate the impact of exercise on CS in human SkM by analyzing muscle biopsies from young, normal-weight individuals and middle-aged individuals with obesity, both before and after exercise intervention.

Methods

Muscle biopsies were collected from both groups before and after an exercise intervention. CS markers, insulin sensitivity (measured with euglycemic clamp), and satellite cell markers were analyzed. Additionally, in vitro experiments were conducted to evaluate the effects of cellular senescence on human satellite cells, focusing on key regulatory genes and insulin signaling.

Results

Individuals with obesity showed significantly elevated CS markers, along with reduced expression of GLUT4 and PAX7, indicating impaired insulin action and regenerative potential. Exercise improved insulin sensitivity, reduced CS markers, and activated satellite cell response in both groups. In vitro experiments revealed that senescence downregulated key regulatory genes in satellite cells and impaired insulin signaling by reducing the Insulin Receptor β-subunit.

Conclusions

These findings highlight the role of CS in regulating insulin sensitivity in SkM and underscore the therapeutic potential of exercise in mitigating age- and obesity-related muscle dysfunction. Targeting CS through exercise or senolytic agents could offer a promising strategy for improving metabolic health and combating sarcopenia, particularly in at-risk populations.

Articles in Press

Physical training reduces cell senescence and associated insulin resistance in skeletal muscle

Agnieszka Podraza-Farhanieh, Rosa Spinelli, Federica Zatterale, Annika Nerstedt, ... Ulf Smith

Physical training reduces cell senescence and associated insulin resistance in skeletal muscle

Background

Cell senescence (CS) is a key aging process that leads to irreversible cell cycle arrest and an altered secretory phenotype. In skeletal muscle (SkM), the accumulation of senescent cells contributes to sarcopenia. Despite exercise being a known intervention for maintaining SkM function and metabolic health, its effects on CS remain poorly understood.

Objectives

This study aimed to investigate the impact of exercise on CS in human SkM by analyzing muscle biopsies from young, normal-weight individuals and middle-aged individuals with obesity, both before and after exercise intervention.

Methods

Muscle biopsies were collected from both groups before and after an exercise intervention. CS markers, insulin sensitivity (measured with euglycemic clamp), and satellite cell markers were analyzed. Additionally, in vitro experiments were conducted to evaluate the effects of cellular senescence on human satellite cells, focusing on key regulatory genes and insulin signaling.

Results

Individuals with obesity showed significantly elevated CS markers, along with reduced expression of GLUT4 and PAX7, indicating impaired insulin action and regenerative potential. Exercise improved insulin sensitivity, reduced CS markers, and activated satellite cell response in both groups. In vitro experiments revealed that senescence downregulated key regulatory genes in satellite cells and impaired insulin signaling by reducing the Insulin Receptor β-subunit.

Conclusions

These findings highlight the role of CS in regulating insulin sensitivity in SkM and underscore the therapeutic potential of exercise in mitigating age- and obesity-related muscle dysfunction. Targeting CS through exercise or senolytic agents could offer a promising strategy for improving metabolic health and combating sarcopenia, particularly in at-risk populations.

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Diabetes Conference 
22-24. Sep, Munich

You are what you eat

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