Biochemical Alterations during the Obese-Aging Process in Female and Male Monosodium Glutamate (MSG)-Treated Mice

Abstract

Obesity, from children to the elderly, has increased in the world at an alarming rate over the past three decades, implying long-term detrimental consequences for individual’s health. Obesity and aging are known to be risk factors for metabolic disorder development, insulin resistance and inflammation, but their relationship is not fully understood. Prevention and appropriate therapies for metabolic disorders and physical disabilities in older adults have become a major public health challenge. Hence, the aim of this study was to evaluate inflammation markers, biochemical parameters and glucose homeostasis during the obese-aging process, to understand the relationship between obesity and health span during the lifetime. In order to do this, the monosodium glutamate (MSG) obesity mice model was used, and data were evaluated at 4, 8, 12, 16 and 20 months in both female and male mice. Our results showed that obesity was a major factor contributing to premature alterations in MSG-treated mice metabolism; however, at older ages, obesity effects were attenuated and MSG-mice became more similar to normal mice. At a younger age (four months old), the Lee index, triglycerides, total cholesterol, TNF-α and transaminases levels increased; while adiponectin decreased and glucose tolerance and insulin sensitivity levels were remarkably altered. However, from 16 months old-on, the Lee index and TNF-α levels diminished significantly, while adiponectin increased, and glucose and insulin homeostasis was recovered. In summary, MSG-treated obese mice showed metabolic changes and differential susceptibility by gender throughout life and during the aging process. Understanding metabolic differences between genders during the lifespan will allow the discovery of specific preventive treatment strategies for chronic diseases and functional decline.

Effect of Nigella Sativa Extract on Inflammatory Cells, Interleukin-10, Interferon-γ and Histological of Kidney in Monosodium Glutamate-Induced Rats

“…Earlier studies, which have also been confirmed this result on more recent reports on the adverse effects of MSG to increase levels of pro-inflammatory cytokines [33,36]. The anti-inflammatory cytokines are series of immunoregulatory molecules that control the pro-inflammatory cytokine response [37].…”

New considerations on hormetic response against oxidative stress

“…Our results showed that during the first 16 months, MSG-mice presented metabolic alterations like higher weight gain, higher Lee index, glucose intolerance, insulin resistance and other biochemical parameters like higher cholesterol and triglycerides levels and IL-6, TNF-α, but lower adiponectin (Hernández-Bautista et al 2014). At tissue level, heart, lung, liver and kidney showed progressive lipoperoxidation and protein carbonylation (manuscript in preparation), however all metabolic and oxidative damages did not show significant differences when compared with control mice after 16 months, and MSG-mice even showed higher adiponectin levels with age.…”

Obesity and related consequences to ageing

“…Chronically elevated levels of pro-inflammatory markers, such as interleukin 6 (IL-6) or tumor necrosis factor-α (TNF-α), are key features of ageing since low-grade inflammatory activity in the elderly is common (Starr et al 2009;Bruunsgaard et al 2001). This pro-inflammatory environment has been defined as Binflammaging.^TNF-α and IL-6 have become frailty markers of ageing in humans (Hernandez-Bautista et al 2014); however, the mechanisms that cause and preserve high levels of these markers in ageing are poorly understood.…”

“…Lower adiponectin concentrations in obese animals were associated with chronic inflammation, increased TNF-α, and altered glucose and insulin homeostasis (Hernandez-Bautista et al 2014). Plasma adiponectin levels, examined in humans, were not only decreased in obese and diabetic subjects but were also inversely associated with measures of insulin resistance (Gulcelik et al 2013).…”