Obesity as a premature aging phenotype — implications for sarcopenic obesity

Emily Nunan, Carson L. Wright, Oluwayemisi A. Semola, Madhan Subramanian, Priya Balasubramanian, Pamela C. Lovern, Ibra S. Fancher, Joshua T. Butcher

Research output: Contribution to journalReview articlepeer-review

1 Scopus citations

Abstract

Obesity and aging have both seen dramatic increases in prevalence throughout society. This review seeks to highlight common pathologies that present with obesity, along with the underlying risk factors, that have remarkable similarity to what is observed in the aged. These include skeletal muscle dysfunction (loss of quantity and quality), significant increases in adiposity, systemic alterations to autonomic dysfunction, reduction in nitric oxide bioavailability, increases in oxidant stress and inflammation, dysregulation of glucose homeostasis, and mitochondrial dysfunction. This review is organized by the aforementioned indices and succinctly highlights literature that demonstrates similarities between the aged and obese phenotypes in both human and animal models. As aging is an inevitability and obesity prevalence is unlikely to significantly decrease in the near future, these two phenotypes will ultimately combine as a multidimensional syndrome (a pathology termed sarcopenic obesity). Whether the pre-mature aging indices accompanying obesity are additive or synergistic upon entering aging is not yet well defined, but the goal of this review is to illustrate the potential consequences of a double aged phenotype in sarcopenic obesity. Clinically, the modifiable risk factors could be targeted specifically in obesity to allow for increased health span in the aged and sarcopenic obese populations.

Original languageEnglish
Pages (from-to)1393-1405
Number of pages13
JournalGeroScience
Volume44
Issue number3
DOIs
StatePublished - Jun 2022

Keywords

  • Aging
  • Diabetes
  • Inflammation
  • Nitric oxide
  • Obesity
  • Oxidant stress
  • Sarcopenic obesity
  • Skeletal muscle

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