Obesity and the dysregulation of fatty acid metabolism: implications for healthy aging

Abstract

Introduction: The population of the world is aging. In 2010, an estimated 524 million people were aged 65 years or older presenting eight percent of the global population. By 2050, this number is expected to 10 nearly triple to approximately 1.5 billion, 16 percent of the world's population. Although people are living longer, the quality of their lives are often compromised due to ill-health. Areas covered: Of the conditions which compromise health as we age, obesity is at the forefront. Over half of the global older population were overweight or obese in 2010, significantly increasing the risk of a range of metabolic diseases. Although, it is well recognised excessive calorie intake is a fundamental 15 driver of adipose tissue dysfunction, the relationship between obesity; intrinsic aging; and fat metabolism is less understood. In this review we discuss the intersection between obesity, aging and the factors which contribute to the dysregulation of whole-body fat metabolism. Expert commentary: Being obese disrupts an array of physiological systems and there is significant crosstalk among these. Moreover it is imperative to acknowledge the contribution intrinsic aging makes 20 to the dysregulation of these systems and the onset of disease.ARTICLE HISTORY

Antioxidants-Related Superoxide Dismutase (SOD), Catalase (CAT), Glutathione Peroxidase (GPX), Glutathione-S-Transferase (GST), and Nitric Oxide Synthase (NOS) Gene Variants Analysis in an Obese Population: A Preliminary Case-Control Study

“…Our enrichment analysis of the studied antioxidant enzymes revealed their implication in several obesity-related pathways and processes such as lipid metabolism/response to lipid processes and dysregulation of fatty acid metabolism [59], cellular biosynthetic process derangement [60], intracellular signal transduction regulation, response to oxidative stress [61], and regulation of blood pressure [62], as shown in Figure 3. rs4880*G allele, (4) SOD3 rs2536512*A allele, (5) GPX1 rs1800668*A allele, and (6) NOS3 rs1799983*G allele.…”

“…Our enrichment analysis of the studied antioxidant enzymes revealed their implication in several obesity-related pathways and processes such as lipid metabolism/response to lipid processes and dysregulation of fatty acid metabolism [59], cellular biosynthetic process derangement [60], intracellular signal transduction regulation, response to oxidative stress [61], and regulation of blood pressure [62], as shown in Figure 3. As a member of phase II drug metabolism-related family catalyst, GSTM1 can detoxify the electrophilic products generated from lipid peroxidation that considers one of the major pathogenic cellular changes in obesity onset and progression [63].…”

Effects of obesity on cholesterol metabolism and its implications for healthy ageing

“…Despite this demographic shift in favour of older individuals, morbidity among this group is high (2) . Many factors make an impact on older people's health; however, an obesity pandemic is emerging as a significant global health concern (3)(4)(5)(6)(7) . Microcosmically, the UK illustrates the extent of the global obesity problem.…”

Modeling cholesterol metabolism and atherosclerosis

“…Cardiovascular disease (CVD) is the number one cause of death globally (Mc Namara et al, 2019). Over the last number of decades several risk factors have been identified for developing CVD, these include elevated low‐density lipoprotein cholesterol (LDL‐C; Ference et al, 2017), physical inactivity (Lachman et al, 2018), genetic predisposition (Berberich & Hegele, 2019), obesity (Cercato & Fonseca, 2019), diabetes mellitus (Einarson et al, 2018), dysregulated fatty acid metabolism (Morgan, Mooney, & Mc Auley, 2016), hypertension (Fuchs & Whelton, 2020), an unhealthy diet (Casas et al, 2018), tobacco smoking (Banks et al, 2019), and excessive alcohol consumption (Toma et al, 2017). Pathophysiologically, CVD is underpinned by atherosclerosis (Figure 1), a chronic inflammatory process defined by a cascade of events which commences with LDL permeating the arterial endothelium and entering the intima (Borén et al, 2020).…”