Strength exercise reduces hepatic pyruvate carboxylase and gluconeogenesis in DIO mice

in Journal of Endocrinology
View More View Less
  • 1 R Pereira, Exercise Cell Biology Lab, Faculty of Applied Sciences, State University of Campinas, Limeira, Brazil
  • 2 K Rodrigues, Exercise Cell Biology Lab, Faculty of Applied Sciences, State University of Campinas, Limeira, Brazil
  • 3 M Sant'Ana, Laboratory of Nutritional Genomics, Faculty of Applied Sciences, State University of Campinas, Limeira, Brazil
  • 4 G Peruca, Exercise Cell Biology Lab, Faculty of Applied Sciences, State University of Campinas, Limeira, Brazil
  • 5 A Morelli, Multidisciplinary Laboratory of Food and Health, Faculty of Applied Sciences, State University of Campinas, Limeira, Brazil
  • 6 F Simabuco, Multidisciplinary Laboratory of Food and Health, Faculty of Applied Sciences, State University of Campinas, Limeira, Brazil
  • 7 A S. R. da Silva, School of Physical Education and Sport of Ribeirão Preto, University of Sao Paulo, Ribeirão Preto, Brazil
  • 8 D Cintra , Laboratory of Nutritional Genomics, Faculty of Applied Sciences, State University of Campinas, Limeira, Brazil
  • 9 E Ropelle, Laboratory of Molecular Biology of Exercise (LaBMEx), Faculty of Applied Sciences, State University of Campinas, Limeira, Brazil
  • 10 J Pauli, Laboratory of Molecular Biology of Exercise (LaBMEx), Faculty of Applied Sciences, State University of Campinas, Limeira, Brazil
  • 11 L de Moura, Exercise Cell Biology Lab, Faculty of Applied Sciences, State University of Campinas, Limeira, Brazil

Correspondence: Leandro de Moura, Email: mouralp@unicamp.br
Restricted access

Obesity is linked to a reduction in the control of hepatic glucose production, which is the primary mechanism related to fasting hyperglycemia and the development of type 2 diabetes mellitus (T2DM). The main system involved in hepatic gluconeogenesis synthesis is controlled by pyruvate carboxylase (PC), which increases in obesity conditions. Recently, we showed that short-term strength training is an important tool against obesity-induced hyperglycemia. As aerobic exercise can reduce the hepatic PC content of obese animals, we hypothesized that strength exercise can also decrease this gluconeogenic enzyme. Therefore, this study investigated whether the metabolic benefits promoted by short-term strength training are related to changes in hepatic PC content. Swiss mice were divided into three groups: lean control (Ctl), obese sedentary (ObS), and obese short-term strength training (STST). The STST protocol was performed through one session/day for 15 days. The obese exercised animals had reduced hyperglycemia and insulin resistance. These results were related to better control of hepatic glucose production and hepatic insulin sensitivity. Our bioinformatics analysis showed that hepatic PC mRNA levels have positive correlations with glucose levels and adiposity, and negative correlations with locomotor activity and muscle mass. We also found that hepatic mRNA levels are related to lipogenic markers in the liver. Finally, we observed that the obese animals had an increased hepatic PC level; however, STST was efficient in reducing its amount. In conclusion, we provide insights into new biomolecular mechanisms by showing how STST is an efficient tool against obesity-related hyperglycemia and T2DM, even without body weight changes.