Effects of High Dietary Carbohydrate and Lipid Intake on the Lifespan of C. elegans

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.

Pediococcus acidilactici CECT9879 (pA1c) Counteracts the Effect of a High-Glucose Exposure in C. elegans by Affecting the Insulin Signaling Pathway (IIS)

“…Moreover, this nematode represents a reliable model to evaluate the effects of high glucose (trying to mimic overfeeding and diabetic conditions) on oxidative stress, aging, and lifespan. In this context, it has been established that a shortened lifespan in high glucose-exposed worms is in part due to the activation of the insulin/IGF-1 signaling (IIS) pathway [ 21 ]. Thus, C. elegans is considered as an appropriate initial screening in vivo model to evaluate the activity of different functional ingredients, including probiotic strains, on fat accumulation, glucose homeostasis, and lifespan, together with elucidating the mechanisms of action.…”

Integrating Transcriptomics and Free Fatty Acid Profiling Analysis Reveal Cu Induces Shortened Lifespan and Increased Fat Accumulation and Oxidative Damage in C. elegans

“…Lipids executed many essential functions, for example, they were efficient energy storage molecules, formed a double-layer membrane structure, and played as signaling molecules [ 48 ]. However, incorrectly lipid homeostasis would develop dysregulated neurological and developmental consequences [ 37 ]; moreover, lipid overload could reduce lifespan of C. elegans [ 37 , 49 ].…”

Anti-hyperglycemic contours of Madhugrit are robustly translated in the Caenorhabditis elegans model of lipid accumulation by regulating oxidative stress and inflammatory response

“…Further evaluations were then performed in vivo on C. elegans . In contrast to in vivo rodent models, the short lifespan of the nematode makes it an ideal model to study the detrimental effects of high glucose exposure ( 76 ). The insulin signaling pathway is conserved across diverse metazoan.…”