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Lipid Metabolism and Metabolic Syndrome

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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: closed (31 August 2021) | Viewed by 51152

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Dr. Montserrat Esteve

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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
Special Issues, Collections and Topics in MDPI journals

Dr. Maria del Mar Romero

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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 Issues, Collections and Topics in MDPI journals

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 Romero
Guest Editors

Manuscript Submission Information

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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 (9 papers)

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Research

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19 pages, 8881 KiB

Open AccessArticle

The Effect of a Sustained High-Fat Diet on the Metabolism of White and Brown Adipose Tissue and Its Impact on Insulin Resistance: A Selected Time Point Cross-Sectional Study

by Babu Raja Maharjan, Susan V. McLennan, Christine Yee, Stephen M. Twigg and Paul F. Williams

Int. J. Mol. Sci. 2021, 22(24), 13639; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222413639 - 20 Dec 2021

Cited by 9 | Viewed by 3162

Abstract

(1) Background: studies on the long-term dynamic changes in fat depot metabolism in response to a high-fat diet (HFD) on hepatic lipid deposition and insulin resistance are sparse. This study investigated the dynamic changes produced by HFD and the production of dysfunctional fat depots on insulin resistance and liver lipid metabolism. (2) Methods: mice fed a chow or HFD (45% kcal fat) diet had three fat depots, liver, and blood collected at 6, 10, 20, and 30 weeks. Anthropometric changes and gene markers for adipogenesis, thermogenesis, ECM remodeling, inflammation, and tissue insulin resistance were measured. (3) Results: early responses to the HFD were increased body weight, minor deposition of lipid in liver, increased adipocyte size, and adipogenesis. Later changes were dysfunctional adipose depots, increased liver fat, insulin resistance (shown by changes in ITT) accompanied by increased inflammatory markers, increased fibrosis (fibrosis > 2-fold, p < 0.05 from week 6), and the presence of crown cells in white fat depots. Later, changes did not increase thermogenic markers in response to the increased calories and decreased UCP1 and PRDM16 proteins in WAT. (4) Conclusions: HFD feeding initially increased adipocyte diameter and number, but later changes caused adipose depots to become dysfunctional, restricting adipose tissue expansion, changing the brown/beige ratios in adipose depots, and causing ectopic lipid deposition and insulin resistance. Full article

(This article belongs to the Special Issue Lipid Metabolism and Metabolic Syndrome)

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13 pages, 1625 KiB

Open AccessArticle

Anti-Obesity Effect of Polygalin C Isolated from Polygala japonica Houtt. via Suppression of the Adipogenic and Lipogenic Factors in 3T3-L1 Adipocytes

by Wona Jee, Seung-Hyeon Lee, Hyun Min Ko, Ji Hoon Jung, Won-Seok Chung and Hyeung-Jin Jang

Int. J. Mol. Sci. 2021, 22(19), 10405; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221910405 - 27 Sep 2021

Cited by 16 | Viewed by 3233

Abstract

Obesity is a risk factor for metabolic diseases including type 2 diabetes, nonalcoholic steatohepatitis (NASH), heart diseases, and cancer. This study aimed to investigate the anti-obesity effect of Polygalin C (PC) isolated from Polygala japonica Houtt. in 3T3-L1 adipocytes. Based on Oil Red O assay results, PC significantly decreased lipid accumulation compared to the control. We found that PC suppressed adipogenesis transcription factors including peroxisome proliferator-activated receptor γ (PPAR γ) and CCAAT/enhancer-binding protein (C/EBP) α, and lipogenic factors such as sterol regulatory element-binding protein 1c (SREBP 1c) and fatty acid synthase (FAS), in 3T3-L1 adipocytes using Western blotting and real-time polymerase chain reaction (PCR). Moreover, PC inhibited the differentiation of 3T3-L1 cells by regulating the AMP-activated protein kinase (AMPK)/acetyl-CoA carboxylase (ACC) and mitogen-activated protein kinase/protein kinase B (MAPK/Akt) signaling pathways. Additionally, we confirmed that PC inhibited early adipogenesis factors C/EBP β and C/EBP δ. Therefore, PC inhibited adipogenesis and lipogenesis in vitro. Thus, PC appears to exert potential therapeutic effects on obesity by suppressing lipid metabolism. Full article

(This article belongs to the Special Issue Lipid Metabolism and Metabolic Syndrome)

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17 pages, 3090 KiB

Open AccessArticle

MicroRNA-126b-5p Exacerbates Development of Adipose Tissue and Diet-Induced Obesity

by Linyuan Shen, Jin He, Ye Zhao, Lili Niu, Lei Chen, Guoqing Tang, Yanzhi Jiang, Xiaoxia Hao, Lin Bai, Xuewei Li, Shunhua Zhang and Li Zhu

Int. J. Mol. Sci. 2021, 22(19), 10261; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms221910261 - 23 Sep 2021

Cited by 8 | Viewed by 2295

Abstract

Obesity has become a worldwide epidemic, caused by many factors such as genetic regulatory elements, unhealthy diet, and lack of exercise. MicroRNAs (miRNAs) are non-coding single-stranded RNA classes, which are about 22 nucleotides in length and highly conserved among species. In the last decade, a series of miRNAs were identified as therapeutic targets for obesity. In the present study, we found that miR-126b-5p was associated with adipogenesis. miR-126b-5p overexpression promoted the proliferation of 3T3-L1 preadipocytes by upregulating the expression of proliferation-related genes and downregulating the expression of apoptosis-related genes; the inhibition of miR-126b-5p gave rise to opposite results. Similarly, miR-126b-5p overexpression could promote the differentiation of 3T3-L1 preadipocytes by increasing the expression of lipid deposition genes and triglyceride (TG) and total cholesterol (TC) levels. Moreover, luciferase reporter assay demonstrated that adiponectin receptor 2 (Adipor2) and acyl-CoA dehydrogenase, long chain (ACADL) were the direct target genes of miR-126b-5p. Moreover, overexpression of miR-126b-5p could exacerbate the clinical symptoms of obesity when mice were induced by a high-fat diet, including increased adipose tissue weight, adipocyte volume, and insulin resistance. Interestingly, overexpression of miR-126b-5p in preadipocytes and mice could significantly increase total fatty acid content and change the fatty acid composition of adipose tissue. Taken together, the present study showed that miR-126b-5p promotes lipid deposition in vivo and in vitro, indicating that miR-126b-5p is a potential target for treating obesity. Full article

(This article belongs to the Special Issue Lipid Metabolism and Metabolic Syndrome)

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17 pages, 5555 KiB

Open AccessArticle

Kaempferol and Kaempferide Attenuate Oleic Acid-Induced Lipid Accumulation and Oxidative Stress in HepG2 Cells

by Fangfang Tie, Jin Ding, Na Hu, Qi Dong, Zhi Chen and Honglun Wang

Int. J. Mol. Sci. 2021, 22(16), 8847; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22168847 - 17 Aug 2021

Cited by 37 | Viewed by 4858

Abstract

Nonalcoholic fatty liver disease (NAFLD) is one of the most common liver diseases which lacks ideal treatment options. Kaempferol and kaempferide, two natural flavonol compounds isolated from Hippophae rhamnoides L., were reported to exhibit a strong regulatory effect on lipid metabolism, for which the mechanism is largely unknown. In the present study, we investigated the effects of kaempferol and kaempferide on oleic acid (OA)-treated HepG2 cells, a widely used in vitro model of NAFLD. The results indicated an increased accumulation of lipid droplets and triacylglycerol (TG) by OA, which was attenuated by kaempferol and kaempferide (5, 10 and 20 μM). Western blot analysis demonstrated that kaempferol and kaempferide reduced expression of lipogenesis-related proteins, including sterol regulatory element-binding protein 1 (SREBP1), fatty acid synthase (FAS) and stearoyl-CoA desaturase 1 (SCD-1). Expression of peroxisome proliferator-activated receptor γ (PPARγ) and CCAAT enhancer binding proteins β (C/EBPβ), two adipogenic transcription factors, was also decreased by kaempferol and kaempferide treatment. In addition, western blot analysis also demonstrated that kaempferol and kaempferide reduced expression of heme oxygenase-1 (HO-1) and nuclear transcription factor-erythroid 2-related factor 2 (Nrf2). Molecular docking was performed to identify the direct molecular targets of kaempferol and kaempferide, and their binding to SCD-1, a critical regulator in lipid metabolism, was revealed. Taken together, our findings demonstrate that kaempferol and kaempferide could attenuate OA-induced lipid accumulation and oxidative stress in HepG2 cells, which might benefit the treatment of NAFLD. Full article

(This article belongs to the Special Issue Lipid Metabolism and Metabolic Syndrome)

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17 pages, 677 KiB

Open AccessArticle

Distinct Fatty Acid Compositions of HDL Phospholipids Are Characteristic of Metabolic Syndrome and Premature Coronary Heart Disease—Family Study

by Timo Paavola, Ulrich Bergmann, Sanna Kuusisto, Sakari Kakko, Markku J. Savolainen and Tuire Salonurmi

Int. J. Mol. Sci. 2021, 22(9), 4908; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094908 - 06 May 2021

Cited by 8 | Viewed by 3251

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 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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14 pages, 1251 KiB

Open AccessArticle

Ovariectomy-Induced Hepatic Lipid and Cytochrome P450 Dysmetabolism Precedes Serum Dyslipidemia

by Hana Malinská, Martina Hüttl, Denisa Miklánková, Jaroslava Trnovská, Iveta Zapletalová, Martin Poruba and Irena Marková

Int. J. Mol. Sci. 2021, 22(9), 4527; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094527 - 26 Apr 2021

Cited by 8 | Viewed by 1888

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 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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35 pages, 4982 KiB

Open AccessReview

The Action of Vitamin D in Adipose Tissue: Is There the Link between Vitamin D Deficiency and Adipose Tissue-Related Metabolic Disorders?

by Izabela Szymczak-Pajor, Krystian Miazek, Anna Selmi, Aneta Balcerczyk and Agnieszka Śliwińska

Int. J. Mol. Sci. 2022, 23(2), 956; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23020956 - 16 Jan 2022

Cited by 45 | Viewed by 11801

Abstract

Adipose tissue plays an important role in systemic metabolism via the secretion of adipocytokines and storing and releasing energy. In obesity, adipose tissue becomes dysfunctional and characterized by hypertrophied adipocytes, increased inflammation, hypoxia, and decreased angiogenesis. Although adipose tissue is one of the major stores of vitamin D, its deficiency is detective in obese subjects. In the presented review, we show how vitamin D regulates numerous processes in adipose tissue and how their dysregulation leads to metabolic disorders. The molecular response to vitamin D in adipose tissue affects not only energy metabolism and adipokine and anti-inflammatory cytokine production via the regulation of gene expression but also genes participating in antioxidant defense, adipocytes differentiation, and apoptosis. Thus, its deficiency disturbs adipocytokines secretion, metabolism, lipid storage, adipogenesis, thermogenesis, the regulation of inflammation, and oxidative stress balance. Restoring the proper functionality of adipose tissue in overweight or obese subjects is of particular importance in order to reduce the risk of developing obesity-related complications, such as cardiovascular diseases and diabetes. Taking into account the results of experimental studies, it seemed that vitamin D may be a remedy for adipose tissue dysfunction, but the results of the clinical trials are not consistent, as some of them show improvement and others no effect of this vitamin on metabolic and insulin resistance parameters. Therefore, further studies are required to evaluate the beneficial effects of vitamin D, especially in overweight and obese subjects, due to the presence of a volumetric dilution of this vitamin among them. Full article

(This article belongs to the Special Issue Lipid Metabolism and Metabolic Syndrome)

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8 pages, 913 KiB

Open AccessReview

The Importance of Food for Endotoxemia and an Inflammatory Response

by Charlotte Erlanson-Albertsson and Karin G. Stenkula

Int. J. Mol. Sci. 2021, 22(17), 9562; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22179562 - 03 Sep 2021

Cited by 8 | Viewed by 4588

Abstract

Bacterial endotoxin is a potent inflammatory antigen abundant in the human intestine. Endotoxins circulate in the blood at low concentrations in all healthy individuals. Elevated levels of circulatory endotoxins may cause inflammation with the development of chronic disease, either affecting metabolism, neurological disease, or resistance to viral and bacterial infections. The most important endotoxin is LPS, being a superantigen. In this narrative review, the effect of various food components to postprandially elevate circulating LPS and inflammatory markers is described. There is evidence that the intake of food enriched in fat, in particular saturated fat, may elevate LPS and pro-inflammatory markers. This occurs in both normal-weight and obese subjects. In obese subjects, inflammatory markers are already elevated before meal consumption. The importance of food choice for endotoxemia and inflammatory response is discussed. Full article

(This article belongs to the Special Issue Lipid Metabolism and Metabolic Syndrome)

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30 pages, 4074 KiB

Open AccessReview

Metabolic Spectrum of Liver Failure in Type 2 Diabetes and Obesity: From NAFLD to NASH to HCC

by Hyunmi Kim, Da Som Lee, Tae Hyeon An, Hyun-Ju Park, Won Kon Kim, Kwang-Hee Bae and Kyoung-Jin Oh

Int. J. Mol. Sci. 2021, 22(9), 4495; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094495 - 26 Apr 2021

Cited by 57 | Viewed by 14198

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 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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