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Adipose Tissue Metabolism in Obesity, Diabetes and Cardiovascular Disease

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

Deadline for manuscript submissions: closed (31 October 2023) | Viewed by 7507

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Special Issue Editor

Prof. Dr. Gary David Lopaschuk

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4-23 Heritage Medical Research Centre, Department of Pediatrics, University of Alberta, Edmonton, AB T6G 2S2, Canada
Interests: obesity; diabetes; insulin; heart disease; cardiology; pharmacology; fatty acids

Special Issue Information

Dear Colleagues,

Obesity and diabetes are important risk factors for the development of cardiovascular disease. Adipose tissue dysfunction is a major contributor to these disease processes. Visceral and epicardial adipose tissue can have endocrine functions and proinflammatory roles that contribute to diabetes and cardiovascular disease, while the thermogenic and endocrine functions of brown adipose tissue have the opposite effect of lessening the severity of cardiovascular disease. Of importance, nutrition-based therapies can improve adipose tissue metabolism and alleviate various proinflammatory processes, oxidative stress, and stress-sensitive signaling pathways. This Special Issue will draw attention to the complex interaction between nutrition, adipose tissue metabolism, obesity, diabetes, and cardiovascular disease.

Prof. Dr. Gary David Lopaschuk
Guest Editor

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Keywords

visceral fat
epicardial fat
brown fat
adipose tissue inflammation
heart failure
cardiovascular disease
nutrition

Published Papers (6 papers)

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Research

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13 pages, 726 KiB

Open AccessArticle

Association between Asymptomatic Hyperuricemia with Adiposity Indices: A Cross-Sectional Study in a Spanish Population

by Carmen Sánchez-Bacaicoa, Esperanza Santano-Mogena, Sergio Rico-Martín, Purificación Rey-Sánchez, Raúl Juárez-Vela, Juan F. Sánchez Muñoz-Torrero, Fidel López-Espuela and Julián F. Calderón-García

Nutrients 2023, 15(22), 4798; https://doi.org/10.3390/nu15224798 - 16 Nov 2023

Viewed by 898

Abstract

Introduction: New anthropometric indices have been developed as an alternative to body mass index (BMI) and waist circumference (WC) to assess body mass and visceral fat. Asymptomatic hyperuricemia is considered an independent cardiovascular risk factor. Currently, little is known about the relationship between asymptomatic hyperuricemia and several new anthropometric indices. This study aimed to assess the association between the presence of asymptomatic hyperuricemia and anthropometric indices, both novel and traditional. Methods: This study analyzed 1094 Spanish subjects who consecutively visited the cardiovascular risk consultation of the University Hospital San Pedro de Alcántara of Cáceres, Spain, between June 2021 and September 2022. Anthropometric measures, including traditional and novel indices, were determined. The asymptomatic hyperuricemia group was defined according to serum uric acid levels. Results: All the anthropometric indices studied, including new and traditional, were significantly greater among patients with asymptomatic hyperuricemia, except for WWI. In multiple linear regression analysis, serum uric acid levels were significantly correlated with BMI, WHR, WHtR, AVI, BAI, BRI, CUN-BAE, and WWI but not ABSI or CI. In the univariate analysis, all indices were associated with asymptomatic hyperuricemia (p < 0.05); however, only WHtR (adjusted OR: 2.93; 95% CI: 1.03–8.37; p = 0.044), AVI (adjusted OR: 1.46; 95% CI: 1.04–2.04; p = 0.026), and BRI (adjusted OR: 1.66; 95% CI: 1.19–2.32; p = 0.003) were significantly associated in multivariate analysis. Finally, WHtR, AVI, and BRI provided the largest AUCs. Conclusions: Our findings showed that WHtR, AVI, and BRI were independently positively associated with asymptomatic hyperuricemia and could be good predictors. Full article

(This article belongs to the Special Issue Adipose Tissue Metabolism in Obesity, Diabetes and Cardiovascular Disease)

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13 pages, 3275 KiB

Open AccessArticle

Cafeteria Diet-Induced Obesity Worsens Experimental CKD

by Jonas Laget, Irene Cortijo, Juliana H. Boukhaled, Karen Muyor, Flore Duranton, Bernard Jover, Fabrice Raynaud, Anne-Dominique Lajoix, Àngel Argilés and Nathalie Gayrard

Nutrients 2023, 15(15), 3331; https://doi.org/10.3390/nu15153331 - 26 Jul 2023

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Abstract

Obesity is a significant risk factor for chronic kidney disease (CKD). This study aimed to evaluate the impact of obesity on the development of kidney fibrosis in a model of cafeteria diet rats undergoing 5/6th nephrectomy (SNx). Collagen 1, 3, and 4 expression, adipocyte size, macrophage number, and the expression of 30 adipokines were determined. Collagen 1 expression in kidney tissue was increased in Standard-SNx and Cafeteria-SNx (7.1 ± 0.6% and 8.9 ± 0.9 tissue area, respectively). Renal expression of collagen 3 and 4 was significantly increased (p < 0.05) in Cafeteria-SNx (8.6 ± 1.5 and 10.9 ± 1.9% tissue area, respectively) compared to Cafeteria (5.2 ± 0.5 and 6.3 ± 0.6% tissue area, respectively). Adipocyte size in eWAT was significantly increased by the cafeteria diet. In Cafeteria-SNx, we observed a significant increase in macrophage number in the kidney (p = 0.01) and a consistent tendency in eWAT. The adipokine level was higher in the Cafeteria groups. Interleukin 11, dipeptidyl peptidase 4, and serpin 1 were increased in Cafeteria-SNx. In the kidney, collagen 3 and 4 expressions and the number of macrophages were increased in Cafeteria-SNx, suggesting an exacerbation by preexisting obesity of CKD-induced renal inflammation and fibrosis. IL11, DPP4, and serpin 1 can act directly on fibrosis and participate in the observed worsening CKD. Full article

(This article belongs to the Special Issue Adipose Tissue Metabolism in Obesity, Diabetes and Cardiovascular Disease)

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14 pages, 2403 KiB

Open AccessArticle

Influence of Gender on Plasma Leptin Levels, Fat Oxidation, and Insulin Sensitivity in Young Adults: The Mediating Role of Fitness and Fatness

by Adrián Montes-de-Oca-García, Alejandro Perez-Bey, Juan Corral-Pérez, Alberto Marín-Galindo, Maria Calderon-Dominguez, Daniel Velázquez-Díaz, Cristina Casals and Jesus G. Ponce-Gonzalez

Nutrients 2023, 15(11), 2628; https://doi.org/10.3390/nu15112628 - 04 Jun 2023

Cited by 1 | Viewed by 1294

Abstract

It is unknown how plasma leptin affects fat oxidation depending on sex in young adults. Therefore, the present cross-sectional study aimed to examine the associations of plasma leptin with resting fat oxidation (RFO), maximal fat oxidation during exercise (MFO), and insulin sensitivity, considering the different responses in men and women, and the mediating role of fatness and cardiorespiratory fitness (CRF). Sixty-five young adults (22.5 ± 4.3 years; body mass index = 25.2 ± 4.7 kg·m⁻², 23 females) participated in this study. Fasting plasma glucose, insulin, and leptin were analyzed. Variables related to insulin resistance (HOMA1-IR, HOMA2-IR), secretion (HOMA-%β), and sensitivity (HOMA-%S, QUICKI) were computed. RFO and MFO were determined through indirect calorimetry. A peak oxygen uptake (VO₂peak) test was performed until exhaustion after the MFO test. The MFO was relativized to body mass (MFO-BM) and the legs’ lean mass divided by the height squared (MFO-LI). In men, leptin was negatively associated with MFO-BM and positively with HOMA-%β (p ≤ 0.02 in both). In women, leptin was positively associated with RFO and QUICKI, and negatively with MFO-BM (p < 0.05 in all). The association between leptin and MFO was mediated by CRF (p < 0.05), but not by fat mass (p > 0.05). Plasma leptin is associated with fat oxidation and insulin secretion/sensitivity, with different responses within each sex. The association between leptin and fat oxidation is mediated by cardiorespiratory fitness. Full article

(This article belongs to the Special Issue Adipose Tissue Metabolism in Obesity, Diabetes and Cardiovascular Disease)

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15 pages, 2778 KiB

Open AccessArticle

PKN1 Kinase: A Key Player in Adipocyte Differentiation and Glucose Metabolism

by Fernando Herrerías-González, Andrée Yeramian, Juan Antonio Baena-Fustegueras, Marta Bueno, Catherine Fleitas, Maricruz de la Fuente, José C. E. Serrano, Ana Granado-Serrano, Maite Santamaría, Nadine Yeramian, Marta Zorzano-Martínez, Conchi Mora and Albert Lecube

Nutrients 2023, 15(10), 2414; https://doi.org/10.3390/nu15102414 - 22 May 2023

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Abstract

Adipocyte dysfunction is the driver of obesity and correlates with insulin resistance and the onset of type 2 diabetes. Protein kinase N1 (PKN1) is a serine/threonine kinase that has been shown to contribute to Glut4 translocation to the membrane and glucose transport. Here, we evaluated the role of PKN1 in glucose metabolism under insulin-resistant conditions in primary visceral adipose tissue (VAT) from 31 patients with obesity and in murine 3T3-L1 adipocytes. In addition, in vitro studies in human VAT samples and mouse adipocytes were conducted to investigate the role of PKN1 in the adipogenic maturation process and glucose homeostasis control. We show that insulin-resistant adipocytes present a decrease in PKN1 activation levels compared to nondiabetic control counterparts. We further show that PKN1 controls the adipogenesis process and glucose metabolism. PKN1-silenced adipocytes present a decrease in both differentiation process and glucose uptake, with a concomitant decrease in the expression levels of adipogenic markers, such as PPARγ, FABP4, adiponectin and CEBPα. Altogether, these results point to PKN1 as a regulator of key signaling pathways involved in adipocyte differentiation and as an emerging player of adipocyte insulin responsiveness. These findings may provide new therapeutic approaches for the management of insulin resistance in type 2 diabetes. Full article

(This article belongs to the Special Issue Adipose Tissue Metabolism in Obesity, Diabetes and Cardiovascular Disease)

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Review

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15 pages, 1230 KiB

Open AccessReview

Glycemic Changes Related to Arsenic Exposure: An Overview of Animal and Human Studies

by Geovanna Beatriz Oliveira Rosendo, Rannapaula Lawrynhuk Urbano Ferreira, Séphora Louyse Silva Aquino, Fernando Barbosa and Lucia Fatima Campos Pedrosa

Nutrients 2024, 16(5), 665; https://doi.org/10.3390/nu16050665 - 27 Feb 2024

Viewed by 679

Abstract

Background: Arsenic (As) is a risk factor associated with glycemic alterations. However, the mechanisms of action and metabolic aspects associated with changes in glycemic profiles have not yet been completely elucidated. Therefore, in this review, we aimed to investigate the metabolic aspects of As and its mechanism of action associated with glycemic changes. Methods: We searched the PubMed (MEDLINE) and Google Scholar databases for relevant articles published in English. A combination of free text and medical subject heading keywords and search terms was used to construct search equations. The search yielded 466 articles; however, only 50 were included in the review. Results: We observed that the relationship between As exposure and glycemic alterations in humans may be associated with sex, smoking status, body mass index, age, occupation, and genetic factors. The main mechanisms of action associated with changes induced by exposure to As in the glycemic profile identified in animals are increased oxidative stress, reduced expression of glucose transporter type 4, induction of inflammatory factor expression and dysfunction of pancreatic β cells. Conclusions: Therefore, As exposure may be associated with glycemic alterations according to inter-individual differences. Full article

(This article belongs to the Special Issue Adipose Tissue Metabolism in Obesity, Diabetes and Cardiovascular Disease)

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28 pages, 1462 KiB

Open AccessReview

Endoplasmic Reticulum Stress and Its Impact on Adipogenesis: Molecular Mechanisms Implicated

by Gyuhui Kim, Jiyoon Lee, Joohun Ha, Insug Kang and Wonchae Choe

Nutrients 2023, 15(24), 5082; https://doi.org/10.3390/nu15245082 - 12 Dec 2023

Viewed by 1778

Abstract

Endoplasmic reticulum (ER) stress plays a pivotal role in adipogenesis, which encompasses the differentiation of adipocytes and lipid accumulation. Sustained ER stress has the potential to disrupt the signaling of the unfolded protein response (UPR), thereby influencing adipogenesis. This comprehensive review illuminates the molecular mechanisms that underpin the interplay between ER stress and adipogenesis. We delve into the dysregulation of UPR pathways, namely, IRE1-XBP1, PERK and ATF6 in relation to adipocyte differentiation, lipid metabolism, and tissue inflammation. Moreover, we scrutinize how ER stress impacts key adipogenic transcription factors such as proliferator-activated receptor γ (PPARγ) and CCAAT-enhancer-binding proteins (C/EBPs) along with their interaction with other signaling pathways. The cellular ramifications include alterations in lipid metabolism, dysregulation of adipokines, and aged adipose tissue inflammation. We also discuss the potential roles the molecular chaperones cyclophilin A and cyclophilin B play in adipogenesis. By shedding light on the intricate relationship between ER stress and adipogenesis, this review paves the way for devising innovative therapeutic interventions. Full article

(This article belongs to the Special Issue Adipose Tissue Metabolism in Obesity, Diabetes and Cardiovascular Disease)

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