Garcia-Roves 2018 MiP2018a

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Pablo Miguel Garcia-Roves
Mitochondrial signature and lifestyle modulation of metabolic plasticity.

Link: MiP2018

Garcia-Roves PM (2018)

Event: MiP2018

COST Action MitoEAGLE

Mitochondrial signature is determined by the nuclear genome, inherited from both parents, and by the mitochondrial genome inherited only from the mother. Through development and differentiation mitochondria adopt their functional properties according to cellular needs. This mitochondrial specialization plays a determinant role in establishing the metabolic plasticity of each cell type and tissue. Metabolic plasticity is considered as the ability of a cell, tissue or organism to modify its metabolism under different physiological and pathological conditions.

During my presentation I would like to demonstrate evidence of differential responses in mitochondrial function and metabolism due to chronic adaptations to exercise practice (healthy lifestyle) and evidence to how metabolic disorders such as obesity and type 2 diabetes modulate mitochondrial function and metabolism in a tissue-specific manner. Finally, systems biology approaches, data integration and tissue-specific analysis has enabled us to identify mitochondria-related metabolic derangements as a key biological process implicated in loss of metabolic plasticity.

Based on the results generated in the previously mentioned studies we conclude that:

  1. An endurance exercise protocol in lean mice promoted an improvement in glycolytic skeletal muscle glucose metabolism, increase in mitochondrial content and mitochondrial respiratory capacity.
  2. The metabolic adaptations promoted by the implementation of the afore mentioned exercise protocol are also observed in formerly obese mice in the context of a lifestyle intervention, therefore, neither the previous pathological conditions nor the calorie restriction hinder this improvement in skeletal muscle oxidative capacity.
  3. In obese diabetic db/db mice, insulin resistance may develop in some tissues such as glycolytic skeletal muscle independently of mitochondrial dysfunction [1].
  4. Mitochondrial respiratory performance is under the control of tissue-specific mechanisms and is not uniformly altered in response to obesity [1].
  5. Under an obesity-related type 2 diabetes phenotype lifestyle intervention significantly reverted the pathological state. However, data integration and tissue-specific analysis highlights an important degree of metabolic irreversibility in white adipose tissue.


Bioblast editor: Plangger M, Kandolf G


Labels: MiParea: Exercise physiology;nutrition;life style  Pathology: Diabetes, Obesity 

Organism: Mouse 






Affiliations

Dept Physiological Sciences, Univ Barcelona Bellvitge Biomedical Research Inst, Spain. - pgarciaroves@ub.edu

References and Support

  1. Holmström MH, Iglesias-Gutierrez E, Zierath JR, Garcia-Roves PM (2012) Tissue-specific control of mitochondrial respiration in obesity-related insulin resistance and diabetes. Am J Physiol Endocrinol Metab 302:E731-9.

Supported by Ramon y Cajal programme 2010-2014, MCIN I+D+i Plan Nacional 2011- reference BFU2011-24679, and Instituto de Salud Carlos III- reference PI15/00701