Abstract
Insulin resistance plays a key role in the development of type 2 diabetes. It arises from a combination of genetic predisposition and environmental and lifestyle factors including lack of physical exercise and poor nutrition habits. The increased risk of type 2 diabetes is molecularly based on defects in insulin signaling, insulin secretion, and inflammation. The present review aims to give an overview on the molecular mechanisms underlying the uptake of glucose and related signaling pathways after acute and chronic exercise. Physical exercise, as crucial part in the prevention and treatment of diabetes, has marked acute and chronic effects on glucose disposal and related inflammatory signaling pathways. Exercise can stimulate molecular signaling pathways leading to glucose transport into the cell. Furthermore, physical exercise has the potential to modulate inflammatory processes by affecting specific inflammatory signaling pathways which can interfere with signaling pathways of the glucose uptake. The intensity of physical training appears to be the primary determinant of the degree of metabolic improvement modulating the molecular signaling pathways in a dose-response pattern, whereas training modality seems to have a secondary role.
Highlights
Insulin resistance plays a key role in the development of type 2 diabetes and is caused by genetic predisposition and environmental and lifestyle factors including physical inactivity and poor nutrition habits [1]
These risk factors contribute to obesity, which is a major determinant of glucometabolic impairment and systemic subclinical inflammation [2]
The overarching aim of this review is to summarize the mechanisms and molecular signaling pathways mediating glucose uptake as well as related changes in the release of immune mediators upon acute and chronic exercise exposure
Summary
Insulin resistance plays a key role in the development of type 2 diabetes and is caused by genetic predisposition and environmental and lifestyle factors including physical inactivity and poor nutrition habits [1]. An insulin-resistant state is associated with changes in immunological and hormonal cross talk involving interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-α), or adiponectin These cytokines and adipokines are part of inflammatory processes and immune defense and can affect molecular signaling pathways modulating glucose uptake. Endurance training imposes a high-frequency (repetition), low-power output demand on muscular contraction, whereas resistance exercise imposes a low-frequency, high-resistance demand [8] These two traditional modalities can be performed as high-intensity training (HIT). We aim to assess the role of training intensity and training modality for the modulation of the aforementioned processes
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