Abstract
Manganese (Mn) is an essential element that is involved in the synthesis and activation of many enzymes and in the regulation of the metabolism of glucose and lipids in humans. In addition, Mn is one of the required components for Mn superoxide dismutase (MnSOD) that is mainly responsible for scavenging reactive oxygen species (ROS) in mitochondrial oxidative stress. Both Mn deficiency and intoxication are associated with adverse metabolic and neuropsychiatric effects. Over the past few decades, the prevalence of metabolic diseases, including type 2 diabetes mellitus (T2MD), obesity, insulin resistance, atherosclerosis, hyperlipidemia, nonalcoholic fatty liver disease (NAFLD), and hepatic steatosis, has increased dramatically. Previous studies have found that ROS generation, oxidative stress, and inflammation are critical for the pathogenesis of metabolic diseases. In addition, deficiency in dietary Mn as well as excessive Mn exposure could increase ROS generation and result in further oxidative stress. However, the relationship between Mn and metabolic diseases is not clear. In this review, we provide insights into the role Mn plays in the prevention and development of metabolic diseases.
Highlights
Manganese (Mn) is an essential element in the human body that is mainly obtained from food and water
We summarize current hypotheses and research to explore the relationship between Mn and metabolic diseases and reveal how Mn affects the metabolism in both molecular biology and population studies
Metabolic diseases are affected by dietary habits, the environment, and genes independently and through their interactions
Summary
Manganese (Mn) is an essential element in the human body that is mainly obtained from food and water. When excessive ROS accumulate abnormally, it would contribute to the oxidative damage found in several neuropathological conditions related to enhanced glucocorticoid expression, which plays an important role in regulating the biosynthesis and metabolism of carbohydrates, lipids, and proteins [14]. MnSOD is the primary antioxidant that scavenges superoxide formed within the mitochondria and protects against oxidative stress [15, 16]. Research in molecular biology or population related to the role of Mn in procession of metabolic diseases via mitochondrial oxidative stress is limited and inconsistent. Induced Mn deficiency caused a number of detrimental effects, such as impaired growth, poor bone formation and skeletal defects, reduced fertility and birth defects, abnormal glucose tolerance, and altered lipid and carbohydrate metabolism in both animals and humans [2]. We summarize current hypotheses and research to explore the relationship between Mn and metabolic diseases and reveal how Mn affects the metabolism in both molecular biology and population studies
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