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Methionine sulfoxide reductase B1 deficiency does not increase high-fat diet-induced insulin resistance in miceстатья
Информация о цитировании статьи получена из
Web of Science,
Scopus
Статья опубликована в журнале из списка Web of Science и/или Scopus
Дата последнего поиска статьи во внешних источниках: 19 декабря 2017 г.
- Авторы: Heo Jung-Yoon, Cha Hye-Na, Young Kim Ki, Lee Eujin, Kim Suk-Jeong, Kim Yong-Woon, Kim Jong-Yeon, Lee In-Kyu, Gladyshev Vadim N., Kim Hwa-Young, Park So-Young
- Журнал: Free Radical Research
- Том: 51
- Номер: 1
- Год издания: 2016
- Издательство: Taylor & Francis
- Местоположение издательства: United Kingdom
- Первая страница: 24
- Последняя страница: 37
- DOI: 10.1080/10715762.2016.1261133
- Аннотация: Methionine-S-sulfoxide reductase (MsrA) protects against high-fat diet-induced insulin resistance due to its antioxidant effects. To determine whether its counterpart, methionine-R-sulfoxide reductase (MsrB) has similar effects, we compared MsrB1 knockout and wild-type mice using a hyperinsulinemic-euglycemic clamp technique. High-fat feeding for eight weeks increased body weights, fat masses, and plasma levels of glucose, insulin, and triglycerides to similar extents in wild-type and MsrB1 knockout mice. Intraperitoneal glucose tolerance test showed no difference in blood glucose levels between the two genotypes after eight weeks on the high-fat diet. The hyperglycemic-euglycemic clamp study showed that glucose infusion rates and whole body glucose uptakes were decreased to similar extents by the high-fat diet in both wild-type and MsrB1 knockout mice. Hepatic glucose production and glucose uptake of skeletal muscle were unaffected by MsrB1 deficiency. The high-fat diet-induced oxidative stress in skeletal muscle and liver was not aggravated in MsrB1-deficient mice. Interestingly, whereas MsrB1 deficiency reduced JNK protein levels to a great extent in skeletal muscle and liver, it markedly elevated phosphorylation of JNK, suggesting the involvement of MsrB1 in JNK protein activation. However, this JNK phosphorylation based on a p-JNK/JNK level did not positively correlate with insulin resistance in MsrB1-deficient mice. Taken together, our results show that, in contrast to MsrA deficiency, MsrB1 deficiency does not increase high-fat diet-induced insulin resistance in mice.
- Добавил в систему: Гладышев Вадим Николаевич