The Role of Exercise in the Interplay between Myokines, Hepatokines, Osteokines, Adipokines, and Modulation of Inflammation for Energy Substrate Redistribution and Fat Mass Loss: A Review

Exercise is an effective strategy for preventing and treating obesity and its related cardiometabolic disorders, resulting in significant loss of body fat mass, white adipose tissue browning, redistribution of energy substrates, optimization of global energy expenditure, enhancement of hypothalamic circuits that control appetite-satiety and energy expenditure, and decreased systemic inflammation and insulin resistance. Novel exercise-inducible soluble factors, including myokines, hepatokines, and osteokines, and immune cytokines and adipokines are hypothesized to play an important role in the body’s response to exercise. To our knowledge, no review has provided a comprehensive integrative overview of these novel molecular players and the mechanisms involved in the redistribution of metabolic fuel during and after exercise, the loss of weight and fat mass, and reduced inflammation. In this review, we explain the potential role of these exercise-inducible factors, namely myokines, such as irisin, IL-6, IL-15, METRNL, BAIBA, and myostatin, and hepatokines, in particular selenoprotein P, fetuin A, FGF21, ANGPTL4, and follistatin. We also describe the function of osteokines, specifically osteocalcin, and of adipokines such as leptin, adiponectin, and resistin. We also emphasize an integrative overview of the pleiotropic mechanisms, the metabolic pathways, and the inter-organ crosstalk involved in energy expenditure, fat mass loss, reduced inflammation, and healthy weight induced by exercise.

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Abstract 17361: How Leptin Harms the Heart in High Fat Diet-Induced Obesity

Circulation ◽

10.1161/circ.142.suppl_3.17361 ◽

2020 ◽

Vol 142 (Suppl_3) ◽

Author(s):

Maria Pini

Keyword(s):

Body Weight ◽

Mass Loss ◽

Fat Mass ◽

High Fat Diet ◽

Cardiac Fibroblasts ◽

High Fat ◽

Wide Range ◽

Plasma Leptin ◽

Fat Mass Loss

Introduction: Sedentary lifestyle and excessive calorie intake are risk factors for CVD. We have demonstrated the cardioprotective effect of exercise in aged mice and the critical role of visceral adiposity and its profibrotic secretome in increasing cardiovascular risks in obesity and aging. The association between exercise, lowered plasma leptin and reduced inflammatory leukocytes has been recently shown in patients with atherosclerosis. It remains unclear whether elevated plasma leptin can preserve or alter cardiovascular function in obesity. Methods: We analyzed the effect of high fat diet (HFD) in C57BL/6J male mice on the heart in terms of function, structure, histology and key molecular markers. Two interventions were used: 1) active fat mass loss via exercise (daily swimming) during HFD; 2) passive fat mass loss via surgical removal of the visceral adipose tissue (VAT lipectomy) followed by HFD. Results: HFD increased body weight and adiposity, leading to higher plasma leptin, glucose and insulin levels, compared to control diet (CD) mice. HFD impaired left ventricle (LV) structure (hypertrophy, interstitial fibrosis) and cardiac function (echocardiography, in vivo hemodynamics). Atria of HFD mice had enhanced pro-inflammatory protein production. Exercise reduced circulating leptin levels in HFD mice by 50%, in line with fat mass loss. In contrast, lipectomy reduced visceral fat mass, but body weight, adiposity and plasma leptin did not change. Both exercise and VAT lipectomy improved cardiac contractility, reversed collagen deposition and oxidative stress in HFD mice. Both interventions downregulated LV pro-inflammatory markers. We proved the role of leptin in cardiac remodeling in vitro by incubating primary cardiac fibroblasts with hyperleptinemic plasma from HFD mice. Remarkably, plasma from HFD-EX (exercise) suppressed the fibro-proliferative and pro-inflammatory responses of cardiac fibroblasts. Conclusions: Leptin directly contribute to cardiac fibrosis in obesity via activation and proliferation of cardiac fibroblasts. Understanding how leptin signals to the heart might have implications in a wide range of CVD, potentially helping early stratification and personalized care.

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PP243-SUN: Outstanding abstract: Higher than 1.2 G/KG/D Protein Intake is Associated with Increased Fat Mass Loss During Weight Loss in Obese Older Adults

Clinical Nutrition ◽

10.1016/s0261-5614(14)50284-1 ◽

2014 ◽

Vol 33 ◽

pp. S110

Author(s):

R. Memelink ◽

A. Verreijen ◽

M. Engberink ◽

P. Weijs

Keyword(s):

Older Adults ◽

Weight Loss ◽

Mass Loss ◽

Fat Mass ◽

Protein Intake ◽

Fat Mass Loss

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Intermittent Fasting and Fat Mass: What Is the Clinical Magnitude?

Obesities ◽

10.3390/obesities2010001 ◽

2022 ◽

Vol 2 (1) ◽

pp. 1-7

Author(s):

Heitor O. Santos

Keyword(s):

Mass Loss ◽

Fat Mass ◽

Clinical Studies ◽

Recent Literature ◽

Energy Restriction ◽

Intermittent Fasting ◽

Reasonable Approach ◽

Treatment Of Obesity ◽

One Year ◽

Fat Mass Loss

Clinical studies addressing the benefits of intermittent fasting (IF) diets have evoked interest in the treatment of obesity. Herein, the overall effects of IF regimens on fat-mass loss are explained in a brief review through a recent literature update. To date, human studies show a reduction in fat mass from 0.7 to 11.3 kg after IF regimens, in which the duration of interventions ranges from two weeks to one year. In light of this, IF regimens can be considered a reasonable approach to weight (fat mass) loss. However, the benefits of IF regimens occur thanks to energy restriction and cannot hence be considered the best dietary protocol compared to conventional diets.

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