Skeletal muscle adiponectin induction depends on diet, muscle type/activity, and exercise modality in C57BL/6 mice

Abstract

Changes in skeletal muscle adiponectin induction have been described in obesity and exercise. However, whether changes are consistent across muscle types and with different exercise modalities, remain unclear. This study compared the effects of diet and two isocaloric training programs on adiponectin induction and its regulators in three muscles: quadriceps (exercising/glycolytic‐oxidative), gastrocnemius (exercising/glycolytic), and masseter (nonexercising/glycolytic). Ten‐week‐old male C57BL/6 mice were fed a high‐fat diet (HFD) (45% fat) or standard CHOW diet (12% fat) ad libitum and underwent one of two training regimes: (1) constant‐moderate training (END), or (2) high intensity interval training (HIIT) for 10 weeks (3 × 40 min sessions/week). Chow and HFD‐fed untrained mice were used as control. Compared with Chow, HFD induced an increase in protein levels of low‐molecular weight (LMW) adiponectin in gastrocnemius and masseter (~2‐fold; P < 0.05), and a decrease of high‐molecular weight adiponectin (HMW‐most bioactive form) in quadriceps (~0.5‐fold; P < 0.05). Only END prevented these changes (P < 0.05). HFD induced a decrease of adiponectin receptor 1 (AdipoR1) protein in exercising muscles of untrained mice (~0.5‐0.8‐fold; P < 0.05); notably, END also decreased AdipoR1 protein levels in lean and HFD mice. This type of training also normalized HFD‐driven mRNA changes found in some adiponectin downstream factors (sirtuin 1, Pgc‐1a, and Ucp2) in the three muscles tested. Our results indicate that diet, muscle type/activity, and exercise modality influences muscle adiponectin profile, and some of its mediators. These parameters should be taken into consideration when investigating this endocrine response of the skeletal muscle, particularly in the context of obesity and metabolic disorders.

Skeletal muscle adiponectin induction in obesity and exercise

“…Moreover, differential responses between AdipoRs have been described after 10 weeks of HFD in C57BL6 mice, where gastrocnemius muscle showed mild increases in protein levels of AdipoR2 (1.3-fold) whereas no changes were seen in AdipoR1 [26]. In contrast, our studies have found consistent decreases of AdipoR1 protein levels (~0.5-fold) after 10 and 20 weeks of HFD in quadriceps and gastrocnemius muscles from mice [32][33][34].…”

“…In a subsequent study, we investigated the effects of 10 weeks of HFD on the adiponectin profile of glycolytic muscles (gastrocnemius and masseter) in mice. Here, increases in LMW adiponectin protein levels (~1.5-fold) were seen without major effects on the HMW isoform [34]. These findings suggest that in order to reach valid conclusions regarding muscle adiponectin induction, the type of muscle analysed, along with analysis of various adiponectin isoforms, are essential requirements for ensuring accurate reporting and interpretation of studies in this field.…”

“…Interestingly, in glycolytic muscles (gastrocnemius and masseter), HFD induced increases in LMW adiponectin, and 10 weeks of constantmoderate exercise normalized this response by reducing this isoform to lean equivalent levels. Furthermore, exercise in the form of running at moderate or high intensities did not change the finding that nonlocomotor muscles, such as masseter did not exhibit HMW adiponectin [34], which suggests that any exercise-induced changes in this isoform are dependent on the intervention and not associated with systemic modifications driven by exercise. In terms of timing of sample collection, it is interesting to highlight that the studies which described increases in AdipoR protein levels collected their samples 24 h after the last training session [26,36].…”

“…These findings highlight the relevance of muscle adiponectin and its signalling when skeletal muscles are challenged to different levels of mechanical loads. In that context, our group has reported that 10 weeks of constant-moderate intensity exercise resulted in significant increases of LMW adiponectin (~1.5-fold) in the gastrocnemius of lean mice [34]. Nevertheless, other studies have reported that soleus muscles from Wistar rats did not exhibit changes in total muscle adiponectin protein after 12 weeks of treadmill training at low, moderate, and high intensities [19], finding that could highlight that the animal model (mouse vs rat, and its respective strains) could have an influence on these outcomes and should be explored.…”

Obesidade associada às reduzidas massa magra e massa óssea: uma emergente e complexa relação envolvendo alterações bioquímicas, metabólicas e funcionais

“…Resumo das variáveis e seus pontos de corte utilizadas para diagnóstico da sarcopenia de acordo com os principais critérios vigentes e osteopenia, sendo considerados potenciais componentes alimentares para o desenvolvimento/manutenção da síndrome100,101 .Além do exposto, tem-se que tanto o tecido adiposo, quanto músculo esquelético e o osso apresentam funções endócrinas, com liberação de citocinas e expressão de receptores para ação destas e de hormônios sintetizados uns pelos outros80 . A seguir são apresentados os principais fatores fisiológicos propostos que intermeiam a fisiopatologia da obesidade osteosarcopênica e o resumo das vias está apresentado na figura 1. possível ocorrência de resistência à adiponectina no músculo esquelético110 . No osso, os efeitos também parecem ser contraditórios, uma vez que estudos in vitro revelaram potencial estímulo à osteoblastogênese111 , enquanto estudos em humanos mostram haver uma relação inversa entre as concentrações dessa citocina e a DMO em mulheres, independente do estado menopausal112 .…”