Abstract
Health and lifespan are influenced by dietary nutrients, whose balance is dependent on the supply or demand of each organism. Many studies have shown that an increased carbohydrate–lipid intake plays a critical role in metabolic dysregulation, which impacts longevity. Caenorhabditis elegans has been successfully used as an in vivo model to study the effects of several factors, such as genetic, environmental, diet, and lifestyle factors, on the molecular mechanisms that have been linked to healthspan, lifespan, and the aging process. There is evidence showing the causative effects of high glucose on lifespan in different diabetic models; however, the precise biological mechanisms affected by dietary nutrients, specifically carbohydrates and lipids, as well as their links with lifespan and longevity, remain unknown. Here, we provide an overview of the deleterious effects caused by high-carbohydrate and high-lipid diets, as well as the molecular signals that affect the lifespan of C. elegans; thus, understanding the detailed molecular mechanisms of high-glucose- and lipid-induced changes in whole organisms would allow the targeting of key regulatory factors to ameliorate metabolic disorders and age-related diseases.
Highlights
It is well known that chronic exposure to elevated glucose or lipids through one’s diet promotes the development of metabolic diseases such as obesity and type 2 diabetes, which may impinge on health-related quality of life
Despite the results mentioned above suggesting that the effects of fructose on the lifespan of C. elegans are due to a high fructose concentration (555 mM), a recent study [118] found that at chronic low-fructose concentrations (5%), wild-type nematodes showed impaired healthspans, as observed by low movement, low food intake, and decreased lifespan
Qi et al showed that treating C. elegans with different ALA concentrations significantly increased the lifespan via the activation of the NHR-49/PPARα and SKN-1/Nrf2 transcription factors, whereby NHR-49 promotes the expression of genes involved in the β-oxidation of lipids, whereas SKN-1 was activated by ALA-derived oxylipins that promote increased longevity resulting from ALA treatment (Table 1, Figure 4) [66]
Summary
It is well known that chronic exposure to elevated glucose or lipids through one’s diet promotes the development of metabolic diseases such as obesity and type 2 diabetes, which may impinge on health-related quality of life. Nowadays, both pathologies have substantial impacts on public health and safety because they exacerbate the burden on health services. The worm C. elegans represents a relevant model for elucidating the regulatory metabolic regulation mechanisms related to carbohydrate and lipid metabolism and can improve the understanding of nutrition-related factors and their impacts on the signaling pathways that are responsible for the development of metabolic disorders, which in consequence modify the human lifespan (Figure 1)
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