Detoxification Enzyme Closely Related to Obesity

Obesity is a state in which excess body fat accumulates to the extent that it may have a negative impact on health. When people’s body mass index (BMI) (measured by dividing a person’s weight by the square of a person’s height) exceeds 30 kg / m 2, people are generally considered obese. Clinical studies have found that obesity not only affects aesthetics, but also increases the likelihood of various diseases and conditions, particularly cardiovascular disease, type 2 diabetes, obstructive sleep apnea, certain types of cancer, osteoarthritis and depression. Obesity is the leading preventable cause of death worldwide, and the incidence of adults and children is rising. In 2015, 600 million adults (12%) and 100 million children were obese in 195 countries. Obesity is more common in women than in men. In 2013, the American Medical Association listed obesity as a disease.

The most common causes of obesity are excessive food intake, lack of physical activity and genetic susceptibility. A small number of cases are mainly caused by genes, endocrine disorders, drug treatment or mental disorders. Recent studies have found that exposure to specific chemicals induce obesity in addition to excessive caloric intake. Further studies have found that this obesity is caused by the inhibition of the expression of the detoxification enzyme, CYP2B, by certain chemicals. CYP2B is a multi-drug bioconverting enzyme. Previous studies have shown that CYP2B gene transcriptional activity is induced in rat liver by a CAR with a zinc finger structure, and CAR is often used by phenobarbital and clotrimazole drugs, poisons and Steroid activation. In humans, Cyp2B6 is widely present in many tissues and organs and is involved in the synthesis and metabolism of a variety of endogenous and exogenous substances. Interestingly, recent studies have shown that inhibition of Cyp2b activity increases dyslipidemia and aging, especially in men.

To investigate the role of Cyp2b in liposome homeostasis and obesity, scientists used wild-type and Cyp2b-deficient mice for 10 weeks on normal (ND) or 60% high-fat diet (HFD) and determined metabolic and molecular changes. The results of the experiment indicated that Cyp2b-null male mice fed HFD were 15% heavier than HFD-fed wild-type mice; however, Cyp2b-null female mice did not show greater body weight. In addition, serum parameters showed that hfc-fed cyp2b-free male mice had elevated levels of ketosis, leptin, and cholesterol compared to wild-type mice. In male Cyp2b-deficient mice, the ratio of liver serum triglycerides was higher than that of wild-type mice fed the same, indicating that Cyp2b plays a role in fatty acid metabolism regardless of diet. Furthermore, RNAseq demonstrated that liver gene expression in ND-fed Cyp2b-depleted male mice was similar to WT male mice fed HFD, suggesting a role for fatty liver disease progression and Cyp2b in liposome homeostasis. Women did not show exemplary changes in liver health and the changes in gene expression were significantly reduced. Therefore, inhibition of CYP2B by exposure to certain chemicals or exposure to chemicals in the workplace may exacerbate metabolic disorders and cause obesity by disrupting fatty acid metabolism.

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