PMID- 35489052 OWN - NLM STAT- MEDLINE DCOM- 20220503 LR - 20220503 IS - 1336-0329 (Electronic) IS - 1210-0668 (Linking) VI - 56 IP - 2 DP - 2022 Apr 30 TI - Bredemolic acid restores glucose utilization and attenuates oxidative stress in palmitic acid-induced insulin-resistant C2C12 cells. PG - 126-133 LID - 10.2478/enr-2022-0014 [doi] AB - Objective. Due to insulin resistance and oxidative stress that are associated with type 2 diabetes mellitus (T2DM), T2DM has become a prevalent metabolic disorder that presents various side effects. However, alternative antidiabetic treatment has commonly been used in treating diabetes mellitus in diabetic patients. In our previous studies, bredemolic acid has been reported as an antidiabetic agent that improves glucose uptake, ameliorates insulin resistance, and oxidative stress in the liver, heart, kidney, and skeletal muscle of prediabetic rats. However, these effects have not been validated in vitro. Therefore, this study was aimed to investigate the effects of bredemolic acid on insulin-mediated glucose utilization, lipid peroxidation, and the total antioxidant capacity (TOAC) in palmitic acid-induced insulin-resistant C2C12 skeletal muscle cells in vitro. Methods. Insulin resistance was induced in the skeletal muscle cells after 4 h of exposure to palmitic acid (0.5 mmol/l). Different cell groups were incubated in culture media DMEM supplemented with fetal calf serum (10%), penicillin/streptomycin (1%), and L-glutamine (1%) and then treated with either insulin (4 microg/ml) or bredemolic acid (12.5 mmol/l) or with both. Thereafter, the cells were seeded in 24- or 96-well plates for determination of the cell viability, glucose utilization, glycogen formation, and antioxidant capacity. Results. The results showed that bredemolic acid significantly improved TOAC and promoted glucose utilization via attenuation of lipid peroxidation and increased glycogen formation in the insulin-resistant cells, respectively. Conclusion. This study showed that bredemolic acid restored the insulin resistance through improved glucose utilization, glycogen formation, and TOAC in the skeletal muscle cells. CI - (c) 2022 Karabo R. Matee et al., published by Sciendo. FAU - Matee, Karabo R AU - Matee KR AD - Department of Physiology, School of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal, College of Health Sciences, Durban, South Africa. FAU - Akinnuga, Akinjide M AU - Akinnuga AM AD - Department of Physiology, School of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal, College of Health Sciences, Durban, South Africa. AD - Department of Physiology, Faculty of Basic Medical Sciences, Cross River University of Technology, Okuku Campus, Yala, Cross River, Nigeria. FAU - Siboto, Angezwa AU - Siboto A AD - Department of Physiology, School of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal, College of Health Sciences, Durban, South Africa. FAU - Ngubane, Phikelelani AU - Ngubane P AD - Department of Physiology, School of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal, College of Health Sciences, Durban, South Africa. FAU - Khathi, Andile AU - Khathi A AD - Department of Physiology, School of Laboratory Medicine and Medical Sciences, University of KwaZulu-Natal, College of Health Sciences, Durban, South Africa. LA - eng PT - Journal Article DEP - 20220430 PL - Germany TA - Endocr Regul JT - Endocrine regulations JID - 9112018 RN - 0 (Antioxidants) RN - 0 (Insulin) RN - 0 (Triterpenes) RN - 2V16EO95H1 (Palmitic Acid) RN - 9005-79-2 (Glycogen) RN - E233J88OHQ (maslinic acid) RN - IY9XDZ35W2 (Glucose) SB - IM MH - Animals MH - Antioxidants/metabolism/pharmacology MH - *Diabetes Mellitus, Type 2/drug therapy/metabolism MH - Glucose/metabolism/pharmacology MH - Glycogen/metabolism MH - Humans MH - Insulin MH - *Insulin Resistance/physiology MH - Oxidative Stress MH - Palmitic Acid/pharmacology/therapeutic use MH - Rats MH - Triterpenes OTO - NOTNLM OT - C2C12 cell OT - bredemolic acid OT - glucose utilization OT - insulin resistance OT - oxidative stress OT - skeletal muscle cell EDAT- 2022/05/01 06:00 MHDA- 2022/05/04 06:00 CRDT- 2022/04/30 13:43 PHST- 2022/04/30 13:43 [entrez] PHST- 2022/05/01 06:00 [pubmed] PHST- 2022/05/04 06:00 [medline] AID - enr-2022-0014 [pii] AID - 10.2478/enr-2022-0014 [doi] PST - epublish SO - Endocr Regul. 2022 Apr 30;56(2):126-133. doi: 10.2478/enr-2022-0014.