The role of tissue oxygenation in obesity-related cardiometabolic complications

被引:0
|
作者
Li, Geng [1 ]
Meex, Ruth C. R. [1 ]
Goossens, Gijs H. [1 ]
机构
[1] Maastricht Univ, Inst Nutr & Translat Res Metab NUTRIM, Dept Human Biol, Med Ctr, POB 616, NL-6200 MD Maastricht, Netherlands
关键词
Obesity; Oxygen; Hypoxia; Metabolism; Insulin resistance; Chronic diseases; SKELETAL-MUSCLE; INSULIN SENSITIVITY; INTERMITTENT HYPOXIA; GLUCOSE-HOMEOSTASIS; INVERSE ASSOCIATION; HUMAN ADIPOCYTES; BLOOD-GLUCOSE; EXPRESSION; METABOLISM; ALTITUDE;
D O I
10.1007/s11154-024-09910-z
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Obesity is a complex, multifactorial, chronic disease that acts as a gateway to a range of other diseases. Evidence from recent studies suggests that changes in oxygen availability in the microenvironment of metabolic organs may exert an important role in the development of obesity-related cardiometabolic complications. In this review, we will first discuss results from observational and controlled laboratory studies that examined the relationship between reduced oxygen availability and obesity-related metabolic derangements. Next, the effects of alterations in oxygen partial pressure (pO2) in the adipose tissue, skeletal muscle and the liver microenvironment on physiological processes in these key metabolic organs will be addressed, and how this might relate to cardiometabolic complications. Since many obesity-related chronic diseases, including type 2 diabetes mellitus, cardiovascular diseases, chronic kidney disease, chronic obstructive pulmonary disease and obstructive sleep apnea, are characterized by changes in pO2 in the tissue microenvironment, a better understanding of the metabolic impact of altered tissue oxygenation can provide valuable insights into the complex interplay between environmental and biological factors involved in the pathophysiology of metabolic impairments. This may ultimately contribute to the development of novel strategies to prevent and treat obesity-related cardiometabolic diseases.
引用
收藏
页码:19 / 30
页数:12
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