Obesity as a premature aging phenotype — implications for sarcopenic obesity

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.

Insights into Pathogenesis, Nutritional and Drug Approach in Sarcopenia: A Systematic Review

“…Myokines can elevate insulin resistance, and mitochondrial dysfunction causes an increase in lipid peroxidation, increasing inflammation, insulin resistance, and oxidative stress, further collaborating with the development of SO [82]. Considering T2DM and SO, it is necessary to prepare physicians, nutritionists, physiotherapists, and physical educators to recognize early sarcopenia and its risk factors in patients with T2DM and to perform appropriate therapeutic approaches capable of preventing and treating this condition [83][84][85][86][87][88].…”

Grape Polyphenols in the Treatment of Human Skeletal Muscle Damage Due to Inflammation and Oxidative Stress during Obesity and Aging: Early Outcomes and Promises

“…Associated with this increase in lifespan, a global obesity epidemic is spreading due to life changes such as inactivity and high-calorie diets, favoring the growth of non-communicable diseases. Obesity and aging are together key risk factors for the development and progression of several chronic/non-communicable diseases (metabolic syndrome, Insulin Resistance (IR), Type 2 Diabetes (T2D) [ 2 , 3 , 4 , 5 , 6 , 7 ], sarcopenia [ 8 , 9 ], and frailty [ 10 ]. The World Health Organization (WHO) defines metabolic syndrome as a pathologic condition characterized by obesity (Body Mass Index (BMI) ≥30 kg/m 2 ), IR, hypertension, and hyperlipidemia [ 11 ]).…”

“…Sarcopenia, defined as a loss of skeletal muscle mass and function [ 8 ], is frequently associated with aging and with a loss of independence, disability, frailty, and compromised quality of life, and, therefore, represents a high risk for morbidity and mortality [ 9 ]. Obese patients could also develop sarcopenia [ 7 ] and with the progression of obesity with aging [ 14 ], a growing number of obese sarcopenic patients is expected. Then, the management of skeletal muscle alteration during obesity and aging is mandatory.…”

“…Indeed, functional and metabolic muscle alterations, as well as skeletal muscle mass decreasing, are all associated with the human mortality rate [ 17 , 18 ]. Then, impairment of skeletal muscle mass and/or function could lead to major pathologies, such as IR, T2D, and to weakness and disability which considerably decrease quality of life and are associated with a higher risk for morbidity and mortality [ 5 , 7 , 19 , 20 ].…”

Differentially Expressed Genes and Molecular Susceptibility to Human Age-Related Diseases

“…Because a standard definition of age-related diseases (ARDs) has yet to be agreed upon, epidemiologists differentiate between, on the one hand, all non-infectious diseases with a reliance on incidence rates rising exponentially with age, no matter the lifespan, and, on the other hand, the diseases that start in early life and have stable or lowered incidence rates in the elderly [ 3 ]. Given this lack of strict classification, many age-related diseases can be named as ARDs: sarcopenic obesity [ 4 ], homeostasis dysregulation [ 5 ], subfertility [ 6 ], lipodystrophy [ 7 ], sarcopenia [ 8 ], macular degeneration [ 9 ], chronic inflammation [ 10 ], osteoarthritis [ 11 ], endothelial dysfunction [ 12 ], tissue senescence [ 13 ], cancer [ 14 ], atherosclerosis [ 15 ], cardiovascular diseases [ 16 ], chronic kidney disease [ 17 ], stroke [ 18 ], frontotemporal dementia [ 19 ], Alzheimer’s [ 20 ], and Parkinson’s [ 21 ], to mention some. Moreover, many other pathologies can contribute to ARDs: amyotrophic lateral sclerosis, to motoneuronal aging [ 22 ]; mitochondrial dysfunction, to aging as such [ 23 ]; vascular atherosclerosis, to cellular senescence [ 24 ]; hypertension, to vascular aging [ 25 ]; thalassemia, to myelodysplastic syndrome [ 26 ]; cancer, to immune system aging and vice versa [ 27 ]; and circadian rhythm disorder, to aging as such [ 28 ].…”