200
ISSN: 2763-5724 / Vol. 04 - n 04 - ano 2024
Ruth C R Meex (2019) explores the relationship between insulin resistance, muscle loss and
type 2 diabetes, highlighting how these factors often coincide, especially in overweight patients.
Obesity and disorders in lipid metabolism play crucial roles in the development of insulin resistance,
particularly due to the increase in the mass of adipose tissue and the dysfunction of this tissue, which
result in a systemic overow of lipids and low -grade inammation, mediated by secretion altered
adipocins and cytokines. The study points out that the increased ow of fatty acids from adipose tissue
contributes to increased fat storage in the liver and skeletal muscle. This can lead to altered secretion
of hepatocinas, mitochondrial dysfunction and insulin signaling compromised in skeletal muscle.
These processes not only exacerbate insulin resistance, but are also associated with the development
of muscle atrophy, suggesting that insulin resistance and muscle loss can be two sides of the same
coin. Although the exact connection between lipid accumulation, type 2 diabetes and muscle atrophy
is still largely unexplored, research suggests that lipid disorders in peripheral tissues such as liver and
skeletal muscle play an important role. These disorders may aect peripheral sensitivity to insulin and
muscle mass through common pathways such as mitochondrial dysfunction and cytokine -mediated
inammation.
G Las (2010) investigates the role of autophagy, a cellular catabolic process, in the health of
pancreatic beta cells and their implication in diabetes. Autophagia, involved in both cellular survival
and cell death, is crucial for adequate insulin secretion and the viability of beta cells. In experimental
models, such as transgenic mice that do not have beta cell autophagia, a decrease in these cells and a
reduction in insulin secretion in response to glucose was observed. Several studies indicate that stress
can stimulate autophagia in beta cells. The increase in the number of autofagosomes was observed
in several in vivo models of diabetes, such as mice DB/DB, mice fed with rich fat diet, PDX-1
Knockout mice, as well as in vitro models of glucotoxicity and lipotoxicity. The pharmacological and
molecular inhibition of autophagia has shown to increase susceptibility to cell stress, suggesting that
autophagia can play a protective role against diabetes relevant stresses. However, recent discoveries
release doubts about these conclusions. In diabetic pancreas and beta cells exposed to fatty acids,