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Special Issue "Lipid Metabolism and Metabolic Syndrome"

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Bioactives and Nutraceuticals".

Deadline for manuscript submissions: 31 August 2021.

Special Issue Editors

Dr. Montserrat Esteve
E-Mail Website
Guest Editor
Department of Biochemistry and Molecular Biomedicine, University of Barcelona, Barcelona, Spain
Interests: Energy metabolism; adipose tissue; obesity; metabolic syndrome; diet induced obesity; food intake; glucorticosteroids; inflammation
Dr. Maria del Mar Romeno
E-Mail Website
Guest Editor
Department of Biochemistry and Molecular Biomedicine, University of Barcelona, Barcelona, Spain
Interests: Nutrition; insulin resistance; metabolic diseases; lipid metabolism; glucose metabolism; obesity; metabolic syndrome; energy metabolism; adipose tissue; adipocytes; intermittent fasting; 11-beta-hydroxysteroid dehydrogenases; food restriction

Special Issue Information

Dear Colleagues,

The increase in global obesity worldwide over the last few decades has become an alarming health problem. Consequently, morbidities associated with obesity, such as type 2 diabetes and cardiovascular diseases, have also increased, the last being the leading cause of death in the world. The association between central obesity, insulin resistance, dyslipidemia, and hypertension is termed metabolic syndrome (MetS). In this environment, an unbalanced diet, with an excess of saturated fats and sugars, plays an important role in the development of MetS, modifying lipid metabolism and promoting the accumulation of visceral fat and the development of fatty liver. The alteration of lipid metabolism eventually leads to insulin resistance and chronic inflammation that characterizes MetS.

This Special Issue aims to focus on recent advances in research and knowledge related to the role of lipid metabolism in any aspect of metabolic syndrome. We welcome original research articles, animal and clinical studies, as well as review articles.

Dr. Montserrat Esteve
Dr. Maria del Mar Romeno
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All papers will be peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Lipid metabolism 
  • Energy metabolism 
  • Obesity 
  • Metabolic syndrome 
  • Adipose tissue 
  • Dyslipidemia 
  • Inflammation 
  • Insulin resistance 
  • Lipotoxicity 
  • Nonalcoholic fatty liver

Published Papers (3 papers)

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Research

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Open AccessArticle
Distinct Fatty Acid Compositions of HDL Phospholipids Are Characteristic of Metabolic Syndrome and Premature Coronary Heart Disease—Family Study
by , , , , and
Int. J. Mol. Sci. 2021, 22(9), 4908; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094908 - 06 May 2021
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Abstract
HDL particles can be structurally modified in atherosclerotic disorders associated with low HDL cholesterol level (HDL-C). We studied whether the lipidome of the main phosphatidylcholine (PC), lysophosphatidylcholine (LPC) and sphingomyelin (SM) species of HDL2 and HDL3 subfractions is associated with premature coronary heart [...] Read more.
HDL particles can be structurally modified in atherosclerotic disorders associated with low HDL cholesterol level (HDL-C). We studied whether the lipidome of the main phosphatidylcholine (PC), lysophosphatidylcholine (LPC) and sphingomyelin (SM) species of HDL2 and HDL3 subfractions is associated with premature coronary heart disease (CHD) or metabolic syndrome (MetS) in families where common low HDL-C predisposes to premature CHD. The lipidome was analyzed by LC-MS. Lysophosphatidylcholines were depleted of linoleic acid relative to more saturated and shorter-chained acids containing species in MetS compared with non-affected subjects: the ratio of palmitic to linoleic acid was elevated by more than 30%. A minor PC (16:0/16:1) was elevated (28–40%) in MetS. The contents of oleic acid containing PCs were elevated relative to linoleic acid containing PCs in MetS; the ratio of PC (16:0/18:1) to PC (16:0/18:2) was elevated by 11–16%. Certain PC and SM ratios, e.g., PC (18:0/20:3) to PC (16:0/18:2) and a minor SM 36:2 to an abundant SM 34:1, were higher (11–36%) in MetS and CHD. The fatty acid composition of certain LPCs and PCs displayed a characteristic pattern in MetS, enriched with palmitic, palmitoleic or oleic acids relative to linoleic acid. Certain PC and SM ratios related consistently to CHD and MetS. Full article
(This article belongs to the Special Issue Lipid Metabolism and Metabolic Syndrome)
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Open AccessArticle
Ovariectomy-Induced Hepatic Lipid and Cytochrome P450 Dysmetabolism Precedes Serum Dyslipidemia
Int. J. Mol. Sci. 2021, 22(9), 4527; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094527 - 26 Apr 2021
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Abstract
Ovarian hormone deficiency leads to increased body weight, visceral adiposity, fatty liver and disorders associated with menopausal metabolic syndrome. To better understand the underlying mechanisms of these disorders in their early phases of development, we investigated the effect of ovariectomy on lipid and [...] Read more.
Ovarian hormone deficiency leads to increased body weight, visceral adiposity, fatty liver and disorders associated with menopausal metabolic syndrome. To better understand the underlying mechanisms of these disorders in their early phases of development, we investigated the effect of ovariectomy on lipid and glucose metabolism. Compared to sham-operated controls, ovariectomized Wistar female rats markedly increased whole body and visceral adipose tissue weight (p ˂ 0.05) and exhibited insulin resistance in peripheral tissues. Severe hepatic triglyceride accumulation (p ˂ 0.001) after ovariectomy preceded changes in both serum lipids and glucose intolerance, reflecting alterations in some CYP proteins. Increased CYP2E1 (p ˂ 0.05) and decreased CYP4A (p ˂ 0.001) after ovariectomy reduced fatty acid oxidation and induced hepatic steatosis. Decreased triglyceride metabolism and secretion from the liver contributed to hepatic triglyceride accumulation in response to ovariectomy. In addition, interscapular brown adipose tissue of ovariectomized rats exhibited decreased fatty acid oxidation (p ˂ 0.01), lipogenesis (p ˂ 0.05) and lipolysis (p ˂ 0.05) despite an increase in tissue weight. The results provide evidence that impaired hepatic triglycerides and dysregulation of some CYP450 proteins may have been involved in the development of hepatic steatosis. The low metabolic activity of brown adipose tissue may have contributed to visceral adiposity as well as triglyceride accumulation during the postmenopausal period. Full article
(This article belongs to the Special Issue Lipid Metabolism and Metabolic Syndrome)
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Review

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Open AccessReview
Metabolic Spectrum of Liver Failure in Type 2 Diabetes and Obesity: From NAFLD to NASH to HCC
Int. J. Mol. Sci. 2021, 22(9), 4495; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094495 - 26 Apr 2021
Viewed by 368
Abstract
Liver disease is the spectrum of liver damage ranging from simple steatosis called as nonalcoholic fatty liver disease (NAFLD) to hepatocellular carcinoma (HCC). Clinically, NAFLD and type 2 diabetes coexist. Type 2 diabetes contributes to biological processes driving the severity of NAFLD, the [...] Read more.
Liver disease is the spectrum of liver damage ranging from simple steatosis called as nonalcoholic fatty liver disease (NAFLD) to hepatocellular carcinoma (HCC). Clinically, NAFLD and type 2 diabetes coexist. Type 2 diabetes contributes to biological processes driving the severity of NAFLD, the primary cause for development of chronic liver diseases. In the last 20 years, the rate of non-viral NAFLD/NASH-derived HCC has been increasing rapidly. As there are currently no suitable drugs for treatment of NAFLD and NASH, a class of thiazolidinediones (TZDs) drugs for the treatment of type 2 diabetes is sometimes used to improve liver failure despite the risk of side effects. Therefore, diagnosis, prevention, and treatment of the development and progression of NAFLD and NASH are important issues. In this review, we will discuss the pathogenesis of NAFLD/NASH and NAFLD/NASH-derived HCC and the current promising pharmacological therapies of NAFLD/NASH. Further, we will provide insights into “adipose-derived adipokines” and “liver-derived hepatokines” as diagnostic and therapeutic targets from NAFLD to HCC. Full article
(This article belongs to the Special Issue Lipid Metabolism and Metabolic Syndrome)
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