scholarly journals Advances in Understanding of the Role of Lipid Metabolism in Aging

Cells ◽  
2021 ◽  
Vol 10 (4) ◽  
pp. 880
Author(s):  
Ki Wung Chung
Keyword(s):  
Lipid Metabolism ◽  
Fatty Acid Utilization ◽  
Body Adiposity ◽  
Excess Adiposity ◽  
Age Related ◽  
Aging Body ◽  
Lipid Metabolites ◽  
Impaired Fatty Acid

During aging, body adiposity increases with changes in the metabolism of lipids and their metabolite levels. Considering lipid metabolism, excess adiposity with increased lipotoxicity leads to various age-related diseases, including cardiovascular disease, cancer, arthritis, type 2 diabetes, and Alzheimer’s disease. However, the multifaceted nature and complexities of lipid metabolism make it difficult to delineate its exact mechanism and role during aging. With advances in genetic engineering techniques, recent studies have demonstrated that changes in lipid metabolism are associated with aging and age-related diseases. Lipid accumulation and impaired fatty acid utilization in organs are associated with pathophysiological phenotypes of aging. Changes in adipokine levels contribute to aging by modulating changes in systemic metabolism and inflammation. Advances in lipidomic techniques have identified changes in lipid profiles that are associated with aging. Although it remains unclear how lipid metabolism is regulated during aging, or how lipid metabolites impact aging, evidence suggests a dynamic role for lipid metabolism and its metabolites as active participants of signaling pathways and regulators of gene expression. This review describes recent advances in our understanding of lipid metabolism in aging, including established findings and recent approaches.

scholarly journals ROLE OF INSULIN IN BRAIN: DELVE INTO THE MOLECULAR MECHANISMS

2021 ◽  
Author(s):  
Sofia Khanam
Keyword(s):  
Molecular Mechanisms ◽  
Insulin Signalling ◽  
Diabetic Patients ◽  
Functional Activities ◽  
Mitochondrial Alterations ◽  
Age Related ◽  
The Brain ◽  
And Oxidative Stress

We have learned over the last several decades that the brain is an important target for insulin action. In central nervous system (CNS) it mainly affects feeding behaviour and various aspects of memory and cognition. Insulin signalling in CNS has emerged as a novel field of research since decreases brain insulin levels and signalling were associated to impaired learning, memory and age-related neurodegenerative diseases. Alterations of these functional activities may contribute to the manifestation of several clinical entities, such as central insulin resistance, type 2 diabetes mellitus (T2DM) and Alzheimer’s disease (AD). A close alliance between T2DM and AD has been reported, to the extent that AD is twice more frequent in diabetic patients. There are links between T2DM and AD through mitochondrial alterations and oxidative stress, altered energy and glucose metabolism, cholesterol modifications, dysfunctional protein O-GlcNAcylation, formation of amyloid plaques, altered Aβ metabolism and tau hyperphosphorylation. Herewith, we aim to integrate the metabolic, neuromodulatory, and neuroprotective roles of insulin in two age-related pathologies: T2DM and AD, both in terms of intracellular signalling and potential therapeutic approach.

scholarly journals Metabolic Adaptations to Aerobic Exercise in Aged Mice

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. 533-533
Author(s):  
Tyler Marx ◽  
Anastasiia Vasileva ◽  
Stephen Hutchison ◽  
Jennifer Stern
Keyword(s):  
Type 2 Diabetes ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Aerobic Exercise Training ◽  
Metabolic Function ◽  
Glucagon Receptor ◽  
Age Related ◽  
Exercise Induced

Abstract Aerobic exercise training is a potent intervention for the treatment and prevention of age-related disease, such as heart disease, obesity, and Type 2 Diabetes. Insulin resistance, a hallmark of Type 2 Diabetes, is reversed in response to aerobic exercise training. However, the effect of aerobic exercise training on glucagon sensitivity is unclear. Glucagon signaling at the liver promotes fatty acid oxidation, inhibits De novo lipogenesis, and activates AMP Kinase, a key mediator of healthy aging. Like humans, aging in mice age leads to a decline in physical and metabolic function. To understand the role of glucagon signaling in exercise-induced improvements in physical and metabolic function in the mouse, we implemented a 16-week aerobic exercise training protocol in young and aged mice. 16 weeks of exercise training initiated at 6 months of age increased markers of physical function (P<0.01) and attenuated age-related weight gain (P<0.05) and fat mass (P<0.0001). Additionally, exercise training improved glucose clearance (P<0.01), enhanced glucose-stimulated insulin secretion (P<0.01) and decreased hepatic lipid accumulation (P<0.05). Importantly, exercise training decreased hypoglycemia stimulated glucagon secretion (P<0.01), with no effect on hepatic glucagon receptor mRNA expression or serum glucagon. Thus, we propose that aerobic exercise training enhances glucagon sensitivity at the liver, implicating glucagon as a potential mediator of exercise-induced improvements in aging. Studies initiating the same aerobic exercise training intervention at 18 months of age in the mouse are currently underway to establish the role of glucagon receptor signaling in exercise-induced improvements in aging.

The Role of Lipids and Lipid Metabolism in Age-Related Macular Degeneration

2019 ◽  
pp. 47-71
Author(s):  
Christopher Fortenbach ◽  
Elissa Goldman ◽  
Amar U. Kishan ◽  
Shilpa Mathew ◽  
Bobeck S. Modjtahedi ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Macular Degeneration ◽  
Age Related Macular Degeneration ◽  
Age Related

scholarly journals Adipose tissue and the insulin resistance syndrome

2001 ◽  
Vol 60 (3) ◽  
pp. 375-380 ◽  
Author(s):  
Keith N. Frayn
Keyword(s):  
Insulin Resistance ◽  
Fatty Acids ◽  
Adipose Tissue ◽  
Insulin Resistance Syndrome ◽  
Fat Storage ◽  
Postprandial Period ◽  
Fat Mobilization ◽  
Lipid Metabolites

Obesity is associated with insulin resistance. Insulin resistance underlies a constellation of adverse metabolic and physiological changes (the insulin resistance syndrome) which is a strong risk factor for development of type 2 diabetes and CHD. The present article discusses how accumulation of triacylglycerol in adipocytes can lead to deterioration of the responsiveness of glucose metabolism in other tissues. Lipodystrophy, lack of adipose tissue, is also associated with insulin resistance. Any plausible explanation for the link between excess adipose tissue and insulin resistance needs to be able to account for this observation. Adipose tissue in obesity becomes refractory to suppression of fat mobilization by insulin, and also to the normal acute stimulatory effect of insulin on activation of lipoprotein lipase (involved in fat storage). The net effect is as though adipocytes are ‘full up’ and resisting further fat storage. Thus, in the postprandial period especially, there is an excess flux of circulating lipid metabolites that would normally have been ‘absorbed’ by adipose tissue. This situation leads to fat deposition in other tissues. Accumulation of triacylglycerol in skeletal muscles and in liver is associated with insulin resistance. In lipodystrophy there is insufficient adipose tissue to absorb the postprandial influx of fatty acids, so these fatty acids will again be directed to other tissues. This view of the link between adipose tissue and insulin resistance emphasises the important role of adipose tissue in ‘buffering’ the daily influx of dietary fat entering the circulation and preventing excessive exposure of other tissues to this influx.

scholarly journals Isoenzyme type 1 of 5alpha-reductase is abundantly transcribed in normal human genital skin fibroblasts and may play an important role in masculinization of 5alpha-reductase type 2 deficient males

2005 ◽  
Vol 152 (6) ◽  
pp. 875-880 ◽  
Author(s):  
Susanne Thiele ◽  
Ute Hoppe ◽  
Paul-Martin Holterhus ◽  
Olaf Hiort
Keyword(s):  
Housekeeping Gene ◽  
Skin Fibroblasts ◽  
Normal Male ◽  
Mrna Concentration ◽  
Age Related ◽  
Normal Human ◽  
Male Genital

Objective: 5alpha-reductase enzymes reduce testosterone (T) to the most potent androgen dihydrotestosterone (DHT). Two isoenzymes are known to day. While the type 2-enzyme (5RII) is predominantly expressed in male genital tissues and mutations are known to cause a severe virilization disorder in genetic males, the role of the type 1-enzyme (5RI) in normal male androgen physiology is unclear. We investigated whether 5RI is transcribed in normal male genital skin fibroblasts (GSFs) and if the transcription is regulated by age or by androgens themselves. Methods: GSF from 14 normally virilized males of different ages, ranging from 8 months to 72 years, obtained at circumcision were cultured. Total RNA was isolated after incubation for 48 h with 100 nM T or without androgens. Each sample was amplified in triplicate by real-time PCR with porphobilinogen desaminase as a housekeeping gene used for semiquantification. Selected cultures were analyzed after incubation with 10 and 100 nM T and 1 and 100 nM DHT for 24, 48 and 120 h. Results: 5RI was transcribed in all investigated samples with a 4.5-fold variability in the mRNA concentration of different individuals. However, neither age-related regulation nor significant influence of T or DHT on the transcription rate was discovered. Conclusion: Since 5RI is abundantly transcribed in GSFs, we hypothesize that this isoenzyme may play important roles in the androgen physiology of normally virilized males and may contribute to masculinization in 5RII-deficient males at the time of puberty.

scholarly journals Gentiopicroside Ameliorates Glucose and Lipid Metabolism in T2DM by Activating PI3K/AKT Pathway Via FGFR1

2021 ◽  
Author(s):  
Zhanchi Xu ◽  
Zeyuan Lin ◽  
Jingran Zeng ◽  
Rui Chen ◽  
Chuting Li ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Glucose Metabolism ◽  
Hepg2 Cells ◽  
Growth Factor Receptor ◽  
Akt Pathway ◽  
Phosphatidylinositol 3 Kinase ◽  
Glucose And Lipid Metabolism ◽  
Lipid Metabolism Disorders

Abstract Background: Abnormalities in lipid and glucose metabolism are are constantly occured in type 2 diabetes (T2DM). However, it can be ameliorated by gentiopicroside (GPS). Considering the key role of fibroblast growth factor receptor 1/phosphatidylinositol 3-kinase/protein kinase B (FGFR1/PI3K/AKT) pathway in T2DM, we explore the possible mechanism of GPS on lipid and glucose metabolism through its effects on FGFR1/PI3K/AKT pathway.Methods: Palmitic acid (PA)-induced HepG2 cells and a db/db mice were used to clarify the role and mechanism of polydatin on lipid and glucose metabolism.Results: GPS ameliorated glucose and lipid metabolism disorders in db/db mice and PA-induced HepG2 cells. Furthermore, GPS activated FGFR1/PI3K/AKT pathway including increased the protein expression of FGFR1 and promoted the phosphorylation of PI3K, AKT and FoxO1. Additionally, knockdown of FGFR1 reversed the activation of PI3K/AKT pathway by GPS.Conclusions: The present study demontrates that GPS ameliorates glucose and lipid metabolism disorders via activation of FGFR1/PI3K/AKT pathway.

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