Lipid Metabolism in Diabetes and Atherosclerosis

A special issue of Nutrients (ISSN 2072-6643). This special issue belongs to the section "Lipids".

Deadline for manuscript submissions: 15 June 2024 | Viewed by 4233

Special Issue Editors


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Guest Editor
1. Department of Internal Medicine, Cardiovascular Research Center, Yale University School of Medicine, New Haven, CT, USA
2. Department of Genetics, Yale School of Medicine, New Haven, CT, USA
Interests: cardiology; genetics; heart; heart defects; congenital; metabolic syndrome; lipid metabolism disorders; hyperlactatemia
Department of Internal Medicine, Cardiovascular Research Center, Yale University School of Medicine, New Haven, CT, USA
Interests: regenerative medicine; cardiovascular; metabolic diseases; lipid metabolism; diabetes

Special Issue Information

Dear Colleagues,

Type II diabetes presents a major healthcare and economic burden affecting nearly 10% of the population worldwide. An overwhelming set of clinical data indicates that people with type II diabetes are more susceptible to developing atherosclerosis. While detailed studies have been conducted on glucose and lipid metabolism in type II diabetes, mechanistic studies that present a causal link between type II diabetes, altered lipid metabolism and atherosclerosis are lacking. Furthermore, how the interplay between signaling and lipid metabolism precipitates into pathological conditions such as atherosclerosis and type II diabetes is not understood. While significant efforts have been made by a diverse group of investigators to tackle this problem, a collective effort is needed to make progress in this area, and this requires close communication between all stakeholders. This Special Issue is dedicated to facilitating communication on this topic. We invite original research articles, review articles, and perspectives from lead investigators on the mechanisms that couple defective signaling with altered lipid metabolism as it relates to atherosclerosis and type II diabetes. This includes, but is not limited to altered insulin/ glucagon signaling, an altered flux of substrates through lipid metabolism pathways, the biogenesis of VLDL, HDL and LDL, the interconversion of lipoproteins, the uptake of lipoproteins and their interaction with glucose homeostasis pathways, and the downstream physiological ramifications. We also solicit articles that discuss therapeutic targets currently in clinical trials or that present novel approaches to mitigate hyperglycemia, hypercholesterolemia, and atherosclerosis.

Prof. Dr. Arya Mani
Dr. Neha Bhat
Guest Editors

Manuscript Submission Information

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Keywords

  • lipid metabolism
  • diabetes
  • atherosclerosis
  • insulin/glucagon signaling
  • lipoproteins
  • hyperglycemia
  • hypercholesterolemia
  • glucose homeostasis pathways

Published Papers (1 paper)

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Review

16 pages, 956 KiB  
Review
Dysregulation of Lipid and Glucose Metabolism in Nonalcoholic Fatty Liver Disease
by Neha Bhat and Arya Mani
Nutrients 2023, 15(10), 2323; https://doi.org/10.3390/nu15102323 - 16 May 2023
Cited by 4 | Viewed by 4035
Abstract
Non-Alcoholic Fatty Liver Disease (NAFLD) is a highly prevalent condition affecting approximately a quarter of the global population. It is associated with increased morbidity, mortality, economic burden, and healthcare costs. The disease is characterized by the accumulation of lipids in the liver, known [...] Read more.
Non-Alcoholic Fatty Liver Disease (NAFLD) is a highly prevalent condition affecting approximately a quarter of the global population. It is associated with increased morbidity, mortality, economic burden, and healthcare costs. The disease is characterized by the accumulation of lipids in the liver, known as steatosis, which can progress to more severe stages such as steatohepatitis, fibrosis, cirrhosis, and even hepatocellular carcinoma (HCC). This review focuses on the mechanisms that contribute to the development of diet-induced steatosis in an insulin-resistant liver. Specifically, it discusses the existing literature on carbon flux through glycolysis, ketogenesis, TCA (Tricarboxylic Acid Cycle), and fatty acid synthesis pathways in NAFLD, as well as the altered canonical insulin signaling and genetic predispositions that lead to the accumulation of diet-induced hepatic fat. Finally, the review discusses the current therapeutic efforts that aim to ameliorate various pathologies associated with NAFLD. Full article
(This article belongs to the Special Issue Lipid Metabolism in Diabetes and Atherosclerosis)
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