Effects of Root Extract of Morinda officinalis in Mice with High-Fat-Diet/Streptozotocin-Induced Diabetes and C2C12 Myoblast Differentiation

Piao Wang; Yi Liu; Tong Zhang; Cheng Yin; Seok Yong Kang; Su Jin Kim; Yong-Ki Park; Hyo Won Jung

doi:10.1021/acsomega.1c03372

Effects of Root Extract of Morinda officinalis in Mice with High-Fat-Diet/Streptozotocin-Induced Diabetes and C2C12 Myoblast Differentiation

ACS Omega. 2021 Oct 11;6(41):26959-26968. doi: 10.1021/acsomega.1c03372. eCollection 2021 Oct 19.

Authors

Piao Wang¹, Yi Liu¹, Tong Zhang¹, Cheng Yin¹, Seok Yong Kang², Su Jin Kim³, Yong-Ki Park^{1

2}, Hyo Won Jung^{1

2}

Affiliations

¹ Department of Herbology, College of Korean Medicine, Dongguk University, 38066 Gyeongju, Korea.
² Korean Medicine R&D Center, Dongguk University, 38066 Gyeongju, Korea.
³ Department of Anesthesiology and Pain Medicine, College of Medicine, Dongguk University, 38066 Gyeongju, Korea.

Abstract

Type 2 diabetes is the most common type of diabetes and causes a decline in muscle quality. In this study, we investigated the effects of the root extract of Morinda officinalis (MORE) on skeletal muscle damage in mice with high-fat-diet (HFD)/streptozotocin (STZ)-induced diabetes and the expression of myogenic and biogenesis regulatory proteins in C2C12 myoblast differentiation. An in vivo model comprised C57BL/6N mice fed HFD for 8 weeks, followed by a single injection of STZ at 120 mg/kg. MORE was administered at 100 and 200 mg/kg once daily (p.o.) for 4 weeks. The changes in body weight, calorie intake, and serum levels of glucose, insulin, total cholesterol (TCHO), HDL-cholesterol (HDL-C), LDL-cholesterol (LDL-C), aspartate transaminase (AST), and alanine aminotransferase (ALT) were investigated in diabetic mice. The histological changes in the gastrocnemius muscle were observed by H&E staining, and then the myofiber size was measured. The expression of the myogenic (MHC, myogenin, and MyoD) and biogenesis (PGC-1α, SIRT1, NRF1, and TFAM) regulatory proteins was examined in the muscle tissues and differentiated C2C12 myoblasts by Western blot, respectively. The administration of MORE at 200 mg/kg in mice with HFD/STZ-induced diabetes significantly reduced weight gains, calorie intake, insulin resistance, and serum levels of glucose, TCHO, LDL-C, AST, and ALT. MORE administration at 100 and 200 mg/kg significantly increased serum insulin and HDL-C levels in diabetic mice. In addition, MORE significantly increased the expression of MHC, myogenin, MyoD, PGC-1α, SIRT1, NRF1, and TFAM in muscle tissues as well as increased the myofiber size in diabetic mice. In C2C12 myoblast differentiation, MORE treatment at 0.5, 1, and 2 mg/mL significantly increased the expression of myogenic and biogenesis regulatory proteins in a dose-dependent manner. MORE improves diabetes symptoms in mice with HFD/STZ-induced diabetes by improving muscle function. This suggests that MORE could be used to prevent or treat diabetes along with muscle disorders.