Transcription of mtDNA and dyslipidemia are ameliorated by aerobic exercise in type 2 diabetes

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Transcription of mtDNA and dyslipidemia are ameliorated by aerobic exercise in type 2 diabetes Sandra Aparecida Benite‑Ribeiro1,2 · Kamila Lauany Lucas‑Lima2 · Jessica N. Jones4 · Julia Matzenbacher dos Santos1,3,4  Received: 8 March 2020 / Accepted: 8 August 2020 © Springer Nature B.V. 2020

Abstract Physical inactivity and unhealthy food intake are strongly associated with the growing prevalence of type 2 diabetes (T2D). Dyslipidemia, a characteristic of T2D patient, contributes to an increase in intra-myocellular lipid accumulation and mitochondria dysfunction, in skeletal muscle cells and further to insulin resistance. The aim of this study was to evaluate the effect of aerobic exercise on dyslipidemia, mitochondrial homeostasis and mitochondrial DNA (mtDNA) transcription in T2D- induced animals. Wistar rats (8 weeks old) were fed a diet containing 60% fat over 9 weeks, at day 14 a single injection of STZ (25 mg/kg) was administered (T2D-induced). At week 3 of the experiment half of the animals started on an aerobic exercise 5-days/week. Blood and soleus muscle were collected at 9th experimental week. Abdominal fat, blood glucose, triglyceride, low-density-lipoprotein and high-density lipoprotein (HDL), and cellular mtDNA copy number, cytochrome b (cytb) mRNA and 8-isoprostane were measured. T2D-induced animals exhibited changes in blood glucose, weight gain, abdominal fat, LDL and muscular 8-isoprostane, mtDNA copy number and cytb mRNA. Aerobic exercise attenuated the increase in weight gain and abdominal fat and the decreased cytb mRNA, and increased HDL. Our results suggest that aerobic exercise might not affect all characteristics related to the development of T2D in the same way. However, since T2D is a multifactorial disease, improvement in parameters such as HDL levels, abdominal fat and weight gain induced by aerobic exercise might delay or inhibit the onset of T2D. Keywords  Type 2 diabetes · Dyslipidemia · Mitochondria · Soleus muscle · Cytochrome b · Aerobic exercise

Introduction Diabetes affects 1 in every 11 people worldwide according to the World Health Organization [1]. Changes in life style such as unhealthy food intake and physical inactivity are strongly associated with the growing prevalence of type 2 diabetes (T2D), which accounts for 95% of diabetic cases [2–4]. Patients developing T2D go through a process * Julia Matzenbacher dos Santos [email protected]; [email protected] 1



Department of Biology, Federal University of Jataí, Jataí, Brazil

2



Postgraduate Program in Animal Bioscience, Federal University of Jataí, Jataí, Brazil

3

Detroit R&D, Inc, Detroit, USA

4

Department of Education, Health and Human Performance, Fairmont State University, 1201 Locust Avenue, Fairmont, WV 26554, USA



initiated by a reduced response to insulin in skeletal muscle and adiposity (insulin resistance) [2, 5]. To compensate insulin resistance and hyperglycemia, pancreatic β-cells overproduce insulin, which over time leads to dysfunction of β-cells and a decre