Literature DB >> 28285649

Pioglitazone-induced improvements in insulin sensitivity occur without concomitant changes in muscle mitochondrial function.

Sudip Bajpeyi1, Magdalena Pasarica2, Kevin E Conley3, Bradley R Newcomer4, Sharon A Jubrias3, Cecilia Gamboa5, Kori Murray6, Olga Sereda6, Lauren M Sparks7, Steven R Smith8.   

Abstract

AIMS: Pioglitazone (Pio) is known to improve insulin sensitivity in skeletal muscle. However, the role of Pio in skeletal muscle lipid metabolism and skeletal muscle oxidative capacity is not clear. The aim of this study was to determine the effects of chronic Pio treatment on skeletal muscle mitochondrial activity in individuals with type 2 diabetes (T2D).
MATERIALS AND METHODS: Twenty-four participants with T2D (13M/11F 53.38±2.1years; BMI 36.47±1.1kg/m2) were randomized to either a placebo (CON, n=8) or a pioglitazone (PIO, n=16) group. Following 12weeks of treatment, we measured insulin sensitivity by hyperinsulinemic-euglycemic clamp (clamp), metabolic flexibility by calculating the change in respiratory quotient (ΔRQ) during the steady state of the clamp, intra- and extra-myocellular lipid content (IMCL and EMCL, respectively) by 1H magnetic resonance spectroscopy (1H-MRS) and muscle maximal ATP synthetic capacity (ATPmax) by 31P-MRS.
RESULTS: Following 12weeks of PIO treatment, insulin sensitivity (p<0.0005 vs. baseline) and metabolic flexibility (p<0.05 vs. CON) significantly increased. PIO treatment significantly decreased IMCL content and increased EMCL content in gastrocnemius, soleus and tibialis anterior muscles. ATPmax was unaffected by PIO treatment.
CONCLUSIONS: These results suggest that 12weeks of pioglitazone treatment improves insulin sensitivity, metabolic flexibility and myocellular lipid distribution without any effect on maximal ATP synthetic capacity in skeletal muscle. Consequently, pioglitazone-induced enhancements in insulin responsiveness and fuel utilization are independent of mitochondrial function.
Copyright © 2016 Elsevier Inc. All rights reserved.

Entities:  

Keywords:  ATPmax; Diabetes; IMCL; Muscle; Pioglitazone

Mesh:

Substances:

Year:  2016        PMID: 28285649     DOI: 10.1016/j.metabol.2016.11.016

Source DB:  PubMed          Journal:  Metabolism        ISSN: 0026-0495            Impact factor:   8.694


  5 in total

Review 1.  Diabetes pharmacotherapy and effects on the musculoskeletal system.

Authors:  Evangelia Kalaitzoglou; John L Fowlkes; Iuliana Popescu; Kathryn M Thrailkill
Journal:  Diabetes Metab Res Rev       Date:  2018-12-20       Impact factor: 4.876

2.  Skeletal muscle energetics are compromised only during high-intensity contractions in the Goto-Kakizaki rat model of type 2 diabetes.

Authors:  Matthew T Lewis; Jonathan D Kasper; Jason N Bazil; Jefferson C Frisbee; Robert W Wiseman
Journal:  Am J Physiol Regul Integr Comp Physiol       Date:  2019-06-12       Impact factor: 3.619

Review 3.  Prescription drugs and mitochondrial metabolism.

Authors:  Cameron A Schmidt
Journal:  Biosci Rep       Date:  2022-04-29       Impact factor: 3.976

Review 4.  Type 2 diabetes subgroups and potential medication strategies in relation to effects on insulin resistance and beta-cell function: A step toward personalised diabetes treatment?

Authors:  Anna Veelen; Edmundo Erazo-Tapia; Jan Oscarsson; Patrick Schrauwen
Journal:  Mol Metab       Date:  2020-12-30       Impact factor: 7.422

5.  Exercise-Induced Improvements in Insulin Sensitivity Are Not Attenuated by a Family History of Type 2 Diabetes.

Authors:  Manuel Amador; Cesar A Meza; Andrew J McAinch; George A King; Jeffrey D Covington; Sudip Bajpeyi
Journal:  Front Endocrinol (Lausanne)       Date:  2020-03-13       Impact factor: 5.555

  5 in total

北京卡尤迪生物科技股份有限公司 © 2022-2023.