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Molecular Research on Obesity and Metabolic Diseases

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: closed (31 August 2019) | Viewed by 38034

Special Issue Editor

Department of Veterinary Bioscience, School of Veterinary Medicine, Nippon Veterinary and Life Science University, 1-7-1 Kyonancho, Musashino, Tokyo 180-8602, Japan
Interests: clinical biochemistry; molecular and biochemical analysis of onset mechanism of obesity and diabetes; comparative endocrinology; nutrition and metabolism in animals; prophylactic veterinary medicine and disease control in animals
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Obesity is the epidmic of the 21st century. In developing countries, the prevalence of obesity continues to rise, and obesity is occurring at younger ages. In 2010, overweight and obesity were estimated to cause 3.4 million deaths, 4% of years of life lost, and 4% of disability-adjusted life-years world wide. The prevalence of overweight and obesity are also increasing in dogs and cats. Obesity and overweight increase the risk of several serious chronic diseases, such as type 2 diabetes, cardiovascular disease, hypertension and stroke, hypercholesterolemia, hypertriglyceridemia, arthritis, asthma, and certain forms of cancer. Obesity is a chronic pro-inflammatory state and associated with immune function. Obesity is associated with inflammation and immune cell recruitment to adipose tissue, muscle, and the intima of atherosclerotic blood vessels. Molecular research on the onset mechanisms of obesity leads early diagnosis of obesity and its associated metabolic diseases. Early diagnosis and treatment of obesity can prevent serious chronic diseases including diabetes mellitus, cancer and others.

This Special Issue will center on reviews and primary data manuscripts that focus on defining: (1) comparative studies in carbohydrate and lipid metabolism in various species; (2) abnormalities in signal transduction related to the onset of obesity and metabolic diseases; (3) metabolic syndrome and lipotoxicity; (4) changes in molecules in obese animals; (5) the detection of new diagnostic molecules for obesity and metabolic diseases, (6) the molecular science of insulin resistance and metabolic syndrome; and (7) new concepts for treating obesity and metabolic diseases.

Prof. Dr. Toshiro Arai
Guest Editor

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Keywords

  • Obesity
  • Metabolic syndrome
  • Insulin resistance
  • Inflammatory cytokines
  • Lipotoxicity
  • Adiponectin
  • Gene expression
  • Cardiovascular disease
  • Lipid metabolism
  • High calorie diet
  • Physical inactivity
  • Macrophage

Published Papers (7 papers)

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Research

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12 pages, 2248 KiB  
Article
Vitamin D Receptor Gene Expression in Adipose Tissue of Obese Individuals is Regulated by miRNA and Correlates with the Pro-Inflammatory Cytokine Level
by Marta Izabela Jonas, Alina Kuryłowicz, Zbigniew Bartoszewicz, Wojciech Lisik, Maurycy Jonas, Krzysztof Kozniewski and Monika Puzianowska-Kuznicka
Int. J. Mol. Sci. 2019, 20(21), 5272; https://doi.org/10.3390/ijms20215272 - 24 Oct 2019
Cited by 30 | Viewed by 3344
Abstract
Background: Given the role that vitamin D (VD) plays in the regulation of the inflammatory activity of adipocytes, we aimed to assess whether obesity changes the expression of VD-related genes in adipose tissue and, if so, to investigate whether this phenomenon depends [...] Read more.
Background: Given the role that vitamin D (VD) plays in the regulation of the inflammatory activity of adipocytes, we aimed to assess whether obesity changes the expression of VD-related genes in adipose tissue and, if so, to investigate whether this phenomenon depends on microRNA interference and how it may influence the local inflammatory milieu. Methods: The expression of genes encoding VD 1α-hydroxylase (CYP27B1), 24-hydroxylase (CYP24A1) and receptor (VDR), selected interleukins and microRNAs was evaluated by real-time PCR in visceral (VAT) and in subcutaneous (SAT) adipose tissues of 55 obese (BMI > 40 kg/m2) and 31 normal-weight (BMI 20–24.9 kg/m2) individuals. Results: VDR mRNA levels were higher, while CYP27B1 levels were lower in adipose tissues of obese patients than in those of normal-weight controls (VAT: P = 0.04, SAT: P < 0.0001 and VAT: P = 0.004, SAT: P = 0.016, respectively). The expression of VDR in VAT of obese subjects correlated negatively with levels of miR-125a-5p (P = 0.0006, rs = −0.525), miR-125b-5p (P = 0.001, rs = −0.495), and miR-214-3p (P = 0.009, rs = −0.379). Additionally, VDR mRNA concentrations in visceral adipose tissues of obese subjects correlated positively with mRNA levels of interleukins: 1β, 6 and 8. Conclusions: We observed obesity-associated up-regulation of VDR and down-regulation of CYP27B mRNA levels in adipose tissue. VDR expression correlates with the expression of pro-inflammatory cytokines and may be regulated by miRNAs. Full article
(This article belongs to the Special Issue Molecular Research on Obesity and Metabolic Diseases)
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6 pages, 361 KiB  
Article
The Ratio of Oxidized Lipoprotein(a) to Native Lipoprotein(a) and the Endothelial Function in Patients with Type 2 Diabetes Mellitus
by Kazuhiko Kotani, Shingo Yamada, Hirokazu Takahashi, Yoshitaka Iwazu and Toshiyuki Yamada
Int. J. Mol. Sci. 2019, 20(19), 4909; https://doi.org/10.3390/ijms20194909 - 03 Oct 2019
Cited by 4 | Viewed by 2103
Abstract
The ratio of oxidized lipoprotein(a) to native lipoprotein(a) (oxLp(a)/Lp(a)) may be a reasonable index for assessing endothelial dysfunction in type 2 diabetes mellitus (T2DM). The present study investigated whether the oxLp(a)/Lp(a) level is correlated with the endothelial function using the Endo-PATTM, [...] Read more.
The ratio of oxidized lipoprotein(a) to native lipoprotein(a) (oxLp(a)/Lp(a)) may be a reasonable index for assessing endothelial dysfunction in type 2 diabetes mellitus (T2DM). The present study investigated whether the oxLp(a)/Lp(a) level is correlated with the endothelial function using the Endo-PATTM, a newly developed device, in patients with T2DM. A total of 63 patients with T2DM (mean age: 59 years old) were enrolled in the study. The patients’ serum Lp(a) and oxLp(a) levels were measured using an enzyme-linked immunosorbent assay. The reactive hyperemia index (RHI) level was measured using an Endo-PATTM 2000. A correlation analysis between the measured variables was conducted. Among the patients, the mean hemoglobin A1c was 7.8%. The median level of oxLp(a)/Lp(a) was 0.28 (interquartile range: 0.07–0.54), and the mean RHI was 1.8 (standard deviation: 0.4). In a multiple linear regression analysis, the oxLp(a)/Lp(a) level was an independent, significant, and inverse variable for the RHI level (β = −0.26, p < 0.05), along with male gender. A high oxLp(a)/Lp(a) level may reflect endothelial dysfunction, as assessed by the Endo-PATTM, in patients with T2DM. Further studies are warranted to confirm the observed findings. Full article
(This article belongs to the Special Issue Molecular Research on Obesity and Metabolic Diseases)
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16 pages, 14948 KiB  
Article
A Proteomics-Based Approach Reveals Differential Regulation of Urine Proteins between Metabolically Healthy and Unhealthy Obese Patients
by Hicham Benabdelkamel, Afshan Masood, Meshail Okla, Mohammed Y. Al-Naami and Assim A. Alfadda
Int. J. Mol. Sci. 2019, 20(19), 4905; https://doi.org/10.3390/ijms20194905 - 03 Oct 2019
Cited by 15 | Viewed by 3060
Abstract
Metabolic dysfunction associated with obesity threatens to inundate health care resources by increasing the incidences of obesity-related diseases. The aim of the present study was to investigate the changes in the urinary proteome of 18 individuals classified into metabolically healthy obese (MHO) and [...] Read more.
Metabolic dysfunction associated with obesity threatens to inundate health care resources by increasing the incidences of obesity-related diseases. The aim of the present study was to investigate the changes in the urinary proteome of 18 individuals classified into metabolically healthy obese (MHO) and metabolically unhealthy obese (MUHO) patients. Proteome analysis was performed using the two-dimensional difference in gel electrophoresis (2D-DIGE) coupled with mass spectrometry (MS). Upon analysis, a total of 54 proteins were found to be affected with ≥1.5-fold change (ANOVA, p ≤ 0.05), of which 44 proteins were upregulated and 10 proteins were downregulated. These differentially abundant proteins were related to nuclear factor κB (NF-κB) and p38 mitogen-activated protein (MAP) kinase pathways and were involved in cellular compromise, inflammatory response, and cancer. Proteins involved in inflammation (fibrinogen alpha (FIBA), serotransferrin (TRFE, and kininogen-1 (KNG1)) and insulin resistance (ADP-ribosylation factor (ARF)-like protein 15 (ARL15) and retinol-binding protein 4 (RET4)) were found to be significantly increased in the urine samples of MUHO compared to MHO patients. Investigating the effects of obesity on urinary proteins can help in developing efficient diagnostic procedures for early detection and prevention of obesity-related complications. Full article
(This article belongs to the Special Issue Molecular Research on Obesity and Metabolic Diseases)
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11 pages, 825 KiB  
Article
Nonalcoholic Fatty Liver Disease (NAFLD), But not Its Susceptibility Gene Variants, Influences the Decrease of Kidney Function in Overweight/Obese Children
by Alessia Di Costanzo, Lucia Pacifico, Laura D’Erasmo, Luca Polito, Michele Di Martino, Francesco Massimo Perla, Ludovica Iezzi, Claudio Chiesa and Marcello Arca
Int. J. Mol. Sci. 2019, 20(18), 4444; https://doi.org/10.3390/ijms20184444 - 09 Sep 2019
Cited by 30 | Viewed by 2777
Abstract
Nonalcoholic fatty liver disease (NAFLD) is associated with an increased risk of kidney disease in adults and children. However, it is uncertain whether this association is influenced by major NAFLD susceptibility genes. In a sample of 230 overweight/obese children, 105 with NAFLD (hepatic [...] Read more.
Nonalcoholic fatty liver disease (NAFLD) is associated with an increased risk of kidney disease in adults and children. However, it is uncertain whether this association is influenced by major NAFLD susceptibility genes. In a sample of 230 overweight/obese children, 105 with NAFLD (hepatic fat fraction ≥5% by magnetic resonance imaging) and 125 without NAFLD, rs738409 in PNPLA3, rs58542926 in TM6SF2, rs1260326 in GCKR, and rs641738 in MBOAT7 were genotyped. Abnormal kidney function was defined as estimated glomerular filtration rate (eGFR) < 90 mL/min/1.73 m2 and/or the presence of microalbuminuria (24 h urinary albumin excretion between 30 and 300 mg). In comparison with children without NAFLD, those with NAFLD showed increased prevalence of reduced eGFR (13.3% vs. 1.6%; p < 0.001) and microalbuminuria (8.6% vs. 3.4%, p = 0.025). TM6SF2, GCKR, and MBOAT7 risk alleles did not show any impact on kidney function, while the PNPLA3 G allele was associated with lower eGFR, but only in children with NAFLD (p = 0.003). After adjustment for confounders, NAFLD (OR, 4.7; 95% CI, 1.5–14.8; padj = 0.007), but not the PNPLA3 gene variant, emerged as the main independent predictor of renal dysfunction. Overall, our findings suggest that NAFLD remains the main determinant of decline in kidney function in overweight/obese children, while the PNPLA3 rs738409 prosteatogenic variant has a small impact, if any. Full article
(This article belongs to the Special Issue Molecular Research on Obesity and Metabolic Diseases)
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15 pages, 5754 KiB  
Article
Participation of NADPH Oxidase-Related Reactive Oxygen Species in Leptin-Promoted Pulmonary Inflammation: Regulation of cPLA2α and COX-2 Expression
by Pei-Sung Hsu, Chia-Mo Lin, Jia-Feng Chang, Chi-Sheng Wu, Kee-Chin Sia, I-Ta Lee, Kuo-Yang Huang and Wei-Ning Lin
Int. J. Mol. Sci. 2019, 20(5), 1078; https://doi.org/10.3390/ijms20051078 - 02 Mar 2019
Cited by 29 | Viewed by 4543
Abstract
Obesity is a worldwide epidemic problem and correlates to varieties of acute or chronic lung diseases such as acute respiratory distress syndrome, chronic obstructive pulmonary disease, and pulmonary fibrosis. An increase of leptin, a kind of adipokine, in lean mice plasma has been [...] Read more.
Obesity is a worldwide epidemic problem and correlates to varieties of acute or chronic lung diseases such as acute respiratory distress syndrome, chronic obstructive pulmonary disease, and pulmonary fibrosis. An increase of leptin, a kind of adipokine, in lean mice plasma has been found to impair immune responses and facilitate the infection of Klebsiella pneumoniae, resulting in increased pneumonia severity. Also, a higher leptin level is found in exhaled breath condensates of obese or asthmatic subjects, compared to healthy ones, suggesting that leptin is involved in the occurrence or exacerbation of lung injury. In previous studies, we showed that leptin stimulated cytosolic phospholipase A2-α (cPLA2α) gene expression in lung alveolar type II cells via mitogen-activated protein kinase (MAPK) and nuclear factor-kappa B (NF-κB)-activated coactivator p300. Herein, we show that the in vivo application of leptin in the respiratory system upregulated the expression of inflammatory proteins cPLA2α and cyclooxygenase-2 (COX-2) together with leukocyte infiltration. Treatment with an ROS scavenger (N-acetylcysteine, NAC), an NADPH oxidase inhibitor (apocynin), or an activating protein (AP)-1 inhibitor (tanshinone IIA) attenuated leptin-mediated cPLA2α/COX-2 expression and leukocyte recruitment in the lung. Leptin increased intracellular oxidative stress in a leptin receptor (OB-R) and NADPH oxidase-dependent manner, leading to the phosphorylation of the AP-1 subunit c-Jun. In summation, leptin increased lung cPLA2α/COX-2 expression and leukocyte recruitment via the NADPH oxidase/ROS/AP-1 pathway. Understanding the inflammatory effects of leptin on the pulmonary system provides opportunities to develop strategies against lung injury related to metabolic syndrome or obesity. Full article
(This article belongs to the Special Issue Molecular Research on Obesity and Metabolic Diseases)
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Review

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22 pages, 1425 KiB  
Review
The Role of Adipose Tissue Mitochondria: Regulation of Mitochondrial Function for the Treatment of Metabolic Diseases
by Jae Ho Lee, Anna Park, Kyoung-Jin Oh, Sang Chul Lee, Won Kon Kim and Kwang-Hee Bae
Int. J. Mol. Sci. 2019, 20(19), 4924; https://doi.org/10.3390/ijms20194924 - 04 Oct 2019
Cited by 154 | Viewed by 12130
Abstract
: Mitochondria play a key role in maintaining energy homeostasis in metabolic tissues, including adipose tissues. The two main types of adipose tissues are the white adipose tissue (WAT) and the brown adipose tissue (BAT). WAT primarily stores excess energy, whereas BAT is [...] Read more.
: Mitochondria play a key role in maintaining energy homeostasis in metabolic tissues, including adipose tissues. The two main types of adipose tissues are the white adipose tissue (WAT) and the brown adipose tissue (BAT). WAT primarily stores excess energy, whereas BAT is predominantly responsible for energy expenditure by non-shivering thermogenesis through the mitochondria. WAT in response to appropriate stimuli such as cold exposure and β-adrenergic agonist undergoes browning wherein it acts as BAT, which is characterized by the presence of a higher number of mitochondria. Mitochondrial dysfunction in adipocytes has been reported to have strong correlation with metabolic diseases, including obesity and type 2 diabetes. Dysfunction of mitochondria results in detrimental effects on adipocyte differentiation, lipid metabolism, insulin sensitivity, oxidative capacity, and thermogenesis, which consequently lead to metabolic diseases. Recent studies have shown that mitochondrial function can be improved by using thiazolidinedione, mitochondria-targeted antioxidants, and dietary natural compounds; by performing exercise; and by controlling caloric restriction, thereby maintaining the metabolic homeostasis by inducing adaptive thermogenesis of BAT and browning of WAT. In this review, we focus on and summarize the molecular regulation involved in the improvement of mitochondrial function in adipose tissues so that strategies can be developed to treat metabolic diseases. Full article
(This article belongs to the Special Issue Molecular Research on Obesity and Metabolic Diseases)
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25 pages, 1089 KiB  
Review
Extracellular Matrix Remodeling of Adipose Tissue in Obesity and Metabolic Diseases
by Francisco Javier Ruiz-Ojeda, Andrea Méndez-Gutiérrez, Concepción María Aguilera and Julio Plaza-Díaz
Int. J. Mol. Sci. 2019, 20(19), 4888; https://doi.org/10.3390/ijms20194888 - 02 Oct 2019
Cited by 142 | Viewed by 8582
Abstract
The extracellular matrix (ECM) is a network of different proteins and proteoglycans that controls differentiation, migration, repair, survival, and development, and it seems that its remodeling is required for healthy adipose tissue expansion. Obesity drives an excessive lipid accumulation in adipocytes, which provokes [...] Read more.
The extracellular matrix (ECM) is a network of different proteins and proteoglycans that controls differentiation, migration, repair, survival, and development, and it seems that its remodeling is required for healthy adipose tissue expansion. Obesity drives an excessive lipid accumulation in adipocytes, which provokes immune cells infiltration, fibrosis (an excess of deposition of ECM components such as collagens, elastin, and fibronectin) and inflammation, considered a consequence of local hypoxia, and ultimately insulin resistance. To understand the mechanism of this process is a challenge to treat the metabolic diseases. This review is focused at identifying the putative role of ECM in adipose tissue, describing its structure and components, its main tissue receptors, and how it is affected in obesity, and subsequently the importance of an appropriate ECM remodeling in adipose tissue expansion to prevent metabolic diseases. Full article
(This article belongs to the Special Issue Molecular Research on Obesity and Metabolic Diseases)
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