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Cells
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Molecular Mechanisms in Metabolic Disease 2022
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Molecular Mechanisms in Metabolic Disease 2022

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Metabolism".

Deadline for manuscript submissions: closed (15 December 2022) | Viewed by 32158

Special Issue Editors

Dr. Louise Torp Dalgaard

E-Mail Website
Guest Editor
Eukaryot Cellebiologi, The Department of Science, Systems and Models, Roskilde University, Universitetsvej 1, 18.2, DK-4000 Roskilde, Denmark
Interests: type 1 diabetes; type 2 diabetes; PCOS; oxidative stress; miRNA
Special Issues, Collections and Topics in MDPI journals
Dr. Anandwardhan A. Hardikar

E-Mail Website
Guest Editor
NHMRC Clinical Trials Centre, Faculty of Medicine and Health, University of Sydney, Sydney, Australia
Interests: ncRNA; diabetes; epigenetics; microbiome; CVD
Dr. Mugdha Joglekar

E-Mail Website
Guest Editor
NHMRC Clinical Trials Centre, Faculty of Medicine and Health, University of Sydney, Sydney, Australia
Interests: miRNA; immunology; diabetes; biomarkers; microbiome
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Metabolic disease refers to a collection of disorders that are related to pathophysiological defects in using and/or converting energy. This includes not only diseases associated with metabolic syndrome but also diseases that are inherited and associated with defects in glucose–insulin metabolism. Although there is a significant body of literature around assessing the biochemical and clinical parameters that are associated with the progression to metabolic disease, in recent years, a body of molecular biomarkers have been unveiled that are not only indicators but also mediators of the pathophysiological processes leading to disease. This Special Issue aims to attract original reports, reviews, meta-analyses/systematic reviews, and short reports on understanding the potential molecular mechanisms underlying metabolic disease. We look forward to submissions that not only demonstrate new molecular mechanisms but also validate the existing research in addition to investigations into biomarkers of processes that lead to metabolic disease. This Special Issue will include articles related to type 1 and 2 diabetes, cardiovascular disease, obesity, lipid disorders, and related manifestations of metabolic syndrome. Submissions related to both existing and future therapies or treatment alternatives for metabolic disease are also welcome.

Dr. Louise Dalgaard
Dr. Anandwardhan A. Hardikar
Dr. Mugdha Joglekar
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 submissions that pass pre-check are 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. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). 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

  • insulin resistance
  • cell therapy
  • epigenetics
  • obesity
  • diabetes
  • CVD
  • ncRNA
  • biomarkers
  • molecular mechanism

Published Papers (9 papers)

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Research

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16 pages, 10861 KiB  
Article
Circulating miRNAs in Women with Polycystic Ovary Syndrome: A Longitudinal Cohort Study
by Pernille B. Udesen, Anja E. Sørensen, Rikke Svendsen, Nanna L. S. Frisk, Anne L. Hess, Mubeena Aziz, Marie Louise M. Wissing, Anne Lis M. Englund and Louise T. Dalgaard
Cells 2023, 12(7), 983; https://0-doi-org.brum.beds.ac.uk/10.3390/cells12070983 - 23 Mar 2023
Cited by 5 | Viewed by 1700
Abstract
Background: Women with polycystic ovary syndrome (PCOS) often change their metabolic profile over time to decrease levels of androgens while often gaining a propensity for the development of the metabolic syndrome. Recent discoveries indicate that microRNAs (miRNAs) play a role in the development [...] Read more.
Background: Women with polycystic ovary syndrome (PCOS) often change their metabolic profile over time to decrease levels of androgens while often gaining a propensity for the development of the metabolic syndrome. Recent discoveries indicate that microRNAs (miRNAs) play a role in the development of PCOS and constitute potential biomarkers for PCOS. We aimed to identify miRNAs associated with the development of an impaired metabolic profile in women with PCOS, in a follow-up study, compared with women without PCOS. Methods and materials: Clinical measurements of PCOS status and metabolic disease were obtained twice 6 years apart in a cohort of 46 women with PCOS and nine controls. All participants were evaluated for degree of metabolic disease (hypertension, dyslipidemia, central obesity, and impaired glucose tolerance). MiRNA levels were measured using Taqman® Array cards of 96 pre-selected miRNAs associated with PCOS and/or metabolic disease. Results: Women with PCOS decreased their levels of androgens during follow-up. Twenty-six of the miRNAs were significantly changed in circulation in women with PCOS during the follow-up, and twenty-four of them had decreased, while levels did not change in the control group. Four miRNAs were significantly different at baseline between healthy controls and women with PCOS; miR-103-3p, miR-139-5p, miR-28-3p, and miR-376a-3p, which were decreased in PCOS. After follow-up, miR-28-3p, miR-139-5p, and miR-376a-3p increased in PCOS women to the levels observed in healthy controls. Of these, miR-139-5p correlated with total testosterone levels (rho = 0.50, padj = 0.013), while miR-376-3p correlated significantly with the waist-hip ratio at follow-up (rho = 0.43, padj = 0.01). Predicted targets of miR-103-3p, miR-139-5p, miR-28-3p, and miR-376a-3p were enriched in pathways associated with Insulin/IGF signaling, interleukin signaling, the GNRH receptor pathways, and other signaling pathways. MiRNAs altered during follow-up in PCOS patients were enriched in pathways related to immune regulation, gonadotropin-releasing hormone signaling, tyrosine kinase signaling, and WNT signaling. Conclusions: These studies indicate that miRNAs associated with PCOS and androgen metabolism overall decrease during a 6-year follow-up, reflecting the phenotypic change in PCOS individuals towards a less hyperandrogenic profile. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Metabolic Disease 2022)
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18 pages, 2209 KiB  
Article
Treatment of VLCAD-Deficient Patient Fibroblasts with Peroxisome Proliferator-Activated Receptor δ Agonist Improves Cellular Bioenergetics
by Olivia M. D’Annibale, Yu Leng Phua, Clinton Van’t Land, Anuradha Karunanidhi, Alejandro Dorenbaum, Al-Walid Mohsen and Jerry Vockley
Cells 2022, 11(17), 2635; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11172635 - 24 Aug 2022
Cited by 3 | Viewed by 2189
Abstract
Background: Very long-chain acyl-CoA dehydrogenase (VLCAD) deficiency is an autosomal recessive disease that prevents the body from utilizing long-chain fatty acids for energy, most needed during stress and fasting. Symptoms can appear from infancy through childhood and adolescence or early adulthood, and include [...] Read more.
Background: Very long-chain acyl-CoA dehydrogenase (VLCAD) deficiency is an autosomal recessive disease that prevents the body from utilizing long-chain fatty acids for energy, most needed during stress and fasting. Symptoms can appear from infancy through childhood and adolescence or early adulthood, and include hypoglycemia, recurrent rhabdomyolysis, myopathy, hepatopathy, and cardiomyopathy. REN001 is a peroxisome-proliferator-activated receptor delta (PPARδ) agonist that modulates the expression of the genes coding for fatty acid β-oxidation enzymes and proteins involved in oxidative phosphorylation. Here, we assessed the effect of REN001 on VLCAD-deficient patient fibroblasts. Methods: VLCAD-deficient patient and control fibroblasts were treated with REN001. Cells were harvested for gene expression analysis, protein content, VLCAD enzyme activity, cellular bioenergetics, and ATP production. Results: VLCAD-deficient cell lines responded differently to REN001 based on genotype. All cells had statistically significant increases in ACADVL gene expression. Small increases in VLCAD protein and enzyme activity were observed and were cell-line- and dose-dependent. Even with these small increases, cellular bioenergetics improved in all cell lines in the presence of REN001, as demonstrated by the oxygen consumption rate and ATP production. VLCAD-deficient cell lines containing missense mutations responded better to REN001 treatment than one containing a duplication mutation in ACADVL. Discussion: Treating VLCAD-deficient fibroblasts with the REN001 PPARδ agonist results in an increase in VLCAD protein and enzyme activity, and a decrease in cellular stress. These results establish REN001 as a potential therapy for VLCADD as enhanced expression may provide a therapeutic increase in total VLCAD activity, but suggest the need for mutation-specific treatment augmented by other treatment measures. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Metabolic Disease 2022)
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18 pages, 1724 KiB  
Article
A Signature of Exaggerated Adipose Tissue Dysfunction in Type 2 Diabetes Is Linked to Low Plasma Adiponectin and Increased Transcriptional Activation of Proteasomal Degradation in Muscle
by Rugivan Sabaratnam, Vibe Skov, Søren K. Paulsen, Stine Juhl, Rikke Kruse, Thea Hansen, Cecilie Halkier, Jonas M. Kristensen, Birgitte F. Vind, Bjørn Richelsen, Steen Knudsen, Jesper Dahlgaard, Henning Beck-Nielsen, Torben A. Kruse and Kurt Højlund
Cells 2022, 11(13), 2005; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11132005 - 23 Jun 2022
Cited by 5 | Viewed by 2460
Abstract
Insulin resistance in skeletal muscle in type 2 diabetes (T2D) is characterized by more pronounced metabolic and molecular defects than in obesity per se. There is increasing evidence that adipose tissue dysfunction contributes to obesity-induced insulin resistance in skeletal muscle. Here, we [...] Read more.
Insulin resistance in skeletal muscle in type 2 diabetes (T2D) is characterized by more pronounced metabolic and molecular defects than in obesity per se. There is increasing evidence that adipose tissue dysfunction contributes to obesity-induced insulin resistance in skeletal muscle. Here, we used an unbiased approach to examine if adipose tissue dysfunction is exaggerated in T2D and linked to diabetes-related mechanisms of insulin resistance in skeletal muscle. Transcriptional profiling and biological pathways analysis were performed in subcutaneous adipose tissue (SAT) and skeletal muscle biopsies from 17 patients with T2D and 19 glucose-tolerant, age and weight-matched obese controls. Findings were validated by qRT-PCR and western blotting of selected genes and proteins. Patients with T2D were more insulin resistant and had lower plasma adiponectin than obese controls. Transcriptional profiling showed downregulation of genes involved in mitochondrial oxidative phosphorylation and the tricarboxylic-acid cycle and increased expression of extracellular matrix (ECM) genes in SAT in T2D, whereas genes involved in proteasomal degradation were upregulated in the skeletal muscle in T2D. qRT-PCR confirmed most of these findings and showed lower expression of adiponectin in SAT and higher expression of myostatin in muscle in T2D. Interestingly, muscle expression of proteasomal genes correlated positively with SAT expression of ECM genes but inversely with the expression of ADIPOQ in SAT and plasma adiponectin. Protein content of proteasomal subunits and major ubiquitin ligases were unaltered in the skeletal muscle of patients with T2D. A transcriptional signature of exaggerated adipose tissue dysfunction in T2D, compared with obesity alone, is linked to low plasma adiponectin and increased transcriptional activation of proteasomal degradation in skeletal muscle. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Metabolic Disease 2022)
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19 pages, 2061 KiB  
Article
The Effect of Ex Vivo Human Serum from Liver Disease Patients on Cellular Protein Synthesis and Growth
by Sophie L. Allen, Alex P. Seabright, Jonathan I. Quinlan, Amritpal Dhaliwal, Felicity R. Williams, Nicholas H. F. Fine, David J. Hodson, Matthew J. Armstrong, Ahmed M. Elsharkaway, Carolyn A. Greig, Yu-Chiang Lai, Janet M. Lord, Gareth G. Lavery and Leigh Breen
Cells 2022, 11(7), 1098; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11071098 - 24 Mar 2022
Cited by 5 | Viewed by 3063
Abstract
Sarcopenia is a common complication affecting liver disease patients, yet the underlying mechanisms remain unclear. We aimed to elucidate the cellular mechanisms that drive sarcopenia progression using an in vitro model of liver disease. C2C12 myotubes were serum and amino acid starved for [...] Read more.
Sarcopenia is a common complication affecting liver disease patients, yet the underlying mechanisms remain unclear. We aimed to elucidate the cellular mechanisms that drive sarcopenia progression using an in vitro model of liver disease. C2C12 myotubes were serum and amino acid starved for 1-h and subsequently conditioned with fasted ex vivo serum from four non-cirrhotic non-alcoholic fatty liver disease patients (NAFLD), four decompensated end-stage liver disease patients (ESLD) and four age-matched healthy controls (CON) for 4- or 24-h. After 4-h C2C12 myotubes were treated with an anabolic stimulus (5 mM leucine) for 30-min. Myotube diameter was reduced following treatment with serum from ESLD compared with CON (−45%) and NAFLD (−35%; p < 0.001 for both). A reduction in maximal mitochondrial respiration (24% and 29%, respectively), coupling efficiency (~12%) and mitophagy (~13%) was identified in myotubes conditioned with NAFLD and ESLD serum compared with CON (p < 0.05 for both). Myostatin (43%, p = 0.04) and MuRF-1 (41%, p = 0.03) protein content was elevated in myotubes treated with ESLD serum compared with CON. Here we highlight a novel, experimental platform to further probe changes in circulating markers associated with liver disease that may drive sarcopenia and develop targeted therapeutic interventions. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Metabolic Disease 2022)
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19 pages, 3255 KiB  
Article
Epiregulin as an Alternative Ligand for Leptin Receptor Alleviates Glucose Intolerance without Change in Obesity
by No-Joon Song, Aejin Lee, Rumana Yasmeen, Qiwen Shen, Kefeng Yang, Shashi Bhushan Kumar, Danah Muhanna, Shanvanth Arnipalli, Sabrena F. Noria, Bradley J. Needleman, Jeffrey W. Hazey, Dean J. Mikami, Joana Ortega-Anaya, Rafael Jiménez-Flores, Jeremy Prokop and Ouliana Ziouzenkova
Cells 2022, 11(3), 425; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11030425 - 26 Jan 2022
Cited by 4 | Viewed by 2775
Abstract
The leptin receptor (LepR) acts as a signaling nexus for the regulation of glucose uptake and obesity, among other metabolic responses. The functional role of LepR under leptin-deficient conditions remains unclear. This study reports that epiregulin (EREG) governed glucose uptake in vitro and [...] Read more.
The leptin receptor (LepR) acts as a signaling nexus for the regulation of glucose uptake and obesity, among other metabolic responses. The functional role of LepR under leptin-deficient conditions remains unclear. This study reports that epiregulin (EREG) governed glucose uptake in vitro and in vivo in Lepob mice by activating LepR under leptin-deficient conditions. Single and long-term treatment with EREG effectively rescued glucose intolerance in comparative insulin and EREG tolerance tests in Lepob mice. The immunoprecipitation study revealed binding between EREG and LepR in adipose tissue of Lepob mice. EREG/LepR regulated glucose uptake without changes in obesity in Lepob mice via mechanisms, including ERK activation and translocation of GLUT4 to the cell surface. EREG-dependent glucose uptake was abolished in Leprdb mice which supports a key role of LepR in this process. In contrast, inhibition of the canonical epidermal growth factor receptor (EGFR) pathway implicated in other EREG responses, increased glucose uptake. Our data provide a basis for understanding glycemic responses of EREG that are dependent on LepR unlike functions mediated by EGFR, including leptin secretion, thermogenesis, pain, growth, and other responses. The computational analysis identified a conserved amino acid sequence, supporting an evolutionary role of EREG as an alternative LepR ligand. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Metabolic Disease 2022)
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17 pages, 2074 KiB  
Article
Effects of Micronutrient Supplementation on Glucose and Hepatic Lipid Metabolism in a Rat Model of Diet Induced Obesity
by Saroj Khatiwada, Virginie Lecomte, Michael F. Fenech, Margaret J. Morris and Christopher A. Maloney
Cells 2021, 10(7), 1751; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10071751 - 11 Jul 2021
Cited by 5 | Viewed by 3651
Abstract
Obesity increases the risk of metabolic disorders, partly through increased oxidative stress. Here, we examined the effects of a dietary micronutrient supplement (consisting of folate, vitamin B6, choline, betaine, and zinc) with antioxidant and methyl donor activities. Male Sprague Dawley rats (3 weeks [...] Read more.
Obesity increases the risk of metabolic disorders, partly through increased oxidative stress. Here, we examined the effects of a dietary micronutrient supplement (consisting of folate, vitamin B6, choline, betaine, and zinc) with antioxidant and methyl donor activities. Male Sprague Dawley rats (3 weeks old, 17/group) were weaned onto control (C) or high-fat diet (HFD) or same diets with added micronutrient supplement (CS; HS). At 14.5 weeks of age, body composition was measured by magnetic resonance imaging. At 21 weeks of age, respiratory quotient and energy expenditure was measured using Comprehensive Lab Animal Monitoring System. At 22 weeks of age, an oral glucose tolerance test (OGTT) was performed, and using fasting glucose and insulin values, Homeostasis Model Assessment of Insulin Resistance (HOMA-IR) was calculated as a surrogate measure of insulin resistance. At 30.5 weeks of age, blood and liver tissues were harvested. Liver antioxidant capacity, lipids and expression of genes involved in lipid metabolism (Cd36, Fabp1, Acaca, Fasn, Cpt1a, Srebf1) were measured. HFD increased adiposity (p < 0.001) and body weight (p < 0.001), both of which did not occur in the HS group. The animals fed HFD developed impaired fasting glucose, impaired glucose tolerance, and fasting hyperinsulinemia compared to control fed animals. Interestingly, HS animals demonstrated an improvement in fasting glucose and fasting insulin. Based on insulin release during OGTT and HOMA-IR, the supplement appeared to reduce the insulin resistance developed by HFD feeding. Supplementation increased hepatic glutathione content (p < 0.05) and reduced hepatic triglyceride accumulation (p < 0.001) regardless of diet; this was accompanied by altered gene expression (particularly of CPT-1). Our findings show that dietary micronutrient supplementation can reduce weight gain and adiposity, improve glucose metabolism, and improve hepatic antioxidant capacity and lipid metabolism in response to HFD intake. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Metabolic Disease 2022)
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19 pages, 893 KiB  
Review
Interferon Family Cytokines in Obesity and Insulin Sensitivity
by Ling-Yu Huang, Chiao-Juno Chiu, Chung-Hsi Hsing and Yu-Hsiang Hsu
Cells 2022, 11(24), 4041; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11244041 - 14 Dec 2022
Cited by 9 | Viewed by 2399
Abstract
Obesity and its associated complications are global public health concerns. Metabolic disturbances and immune dysregulation cause adipose tissue stress and dysfunction in obese individuals. Immune cell accumulation in the adipose microenvironment is the main cause of insulin resistance and metabolic dysfunction. Infiltrated immune [...] Read more.
Obesity and its associated complications are global public health concerns. Metabolic disturbances and immune dysregulation cause adipose tissue stress and dysfunction in obese individuals. Immune cell accumulation in the adipose microenvironment is the main cause of insulin resistance and metabolic dysfunction. Infiltrated immune cells, adipocytes, and stromal cells are all involved in the production of proinflammatory cytokines and chemokines in adipose tissues and affect systemic homeostasis. Interferons (IFNs) are a large family of pleiotropic cytokines that play a pivotal role in host antiviral defenses. IFNs are critical immune modulators in response to pathogens, dead cells, and several inflammation-mediated diseases. Several studies have indicated that IFNs are involved in the pathogenesis of obesity. In this review, we discuss the roles of IFN family cytokines in the development of obesity-induced inflammation and insulin resistance. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Metabolic Disease 2022)
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13 pages, 648 KiB  
Review
Pancreatic Transdifferentiation Using β-Cell Transcription Factors for Type 1 Diabetes Treatment
by Alexandra L. G. Mahoney, Najah T. Nassif, Bronwyn A. O’Brien and Ann M. Simpson
Cells 2022, 11(14), 2145; https://0-doi-org.brum.beds.ac.uk/10.3390/cells11142145 - 08 Jul 2022
Cited by 3 | Viewed by 2348
Abstract
Type 1 diabetes is a chronic illness in which the native beta (β)-cell population responsible for insulin release has been the subject of autoimmune destruction. This condition requires patients to frequently measure their blood glucose concentration and administer multiple daily exogenous insulin injections [...] Read more.
Type 1 diabetes is a chronic illness in which the native beta (β)-cell population responsible for insulin release has been the subject of autoimmune destruction. This condition requires patients to frequently measure their blood glucose concentration and administer multiple daily exogenous insulin injections accordingly. Current treatments fail to effectively treat the disease without significant side effects, and this has led to the exploration of different approaches for its treatment. Gene therapy and the use of viral vectors has been explored extensively and has been successful in treating a range of diseases. The use of viral vectors to deliver β-cell transcription factors has been researched in the context of type 1 diabetes to induce the pancreatic transdifferentiation of cells to replace the β-cell population destroyed in patients. Studies have used various combinations of pancreatic and β-cell transcription factors in order to induce pancreatic transdifferentiation and have achieved varying levels of success. This review will outline why pancreatic transcription factors have been utilised and how their application can allow the development of insulin-producing cells from non β-cells and potentially act as a cure for type 1 diabetes. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Metabolic Disease 2022)
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38 pages, 1762 KiB  
Review
Metabolomics in Diabetes and Diabetic Complications: Insights from Epidemiological Studies
by Qiao Jin and Ronald Ching Wan Ma
Cells 2021, 10(11), 2832; https://0-doi-org.brum.beds.ac.uk/10.3390/cells10112832 - 21 Oct 2021
Cited by 70 | Viewed by 9858
Abstract
The increasing prevalence of diabetes and its complications, such as cardiovascular and kidney disease, remains a huge burden globally. Identification of biomarkers for the screening, diagnosis, and prognosis of diabetes and its complications and better understanding of the molecular pathways involved in the [...] Read more.
The increasing prevalence of diabetes and its complications, such as cardiovascular and kidney disease, remains a huge burden globally. Identification of biomarkers for the screening, diagnosis, and prognosis of diabetes and its complications and better understanding of the molecular pathways involved in the development and progression of diabetes can facilitate individualized prevention and treatment. With the advancement of analytical techniques, metabolomics can identify and quantify multiple biomarkers simultaneously in a high-throughput manner. Providing information on underlying metabolic pathways, metabolomics can further identify mechanisms of diabetes and its progression. The application of metabolomics in epidemiological studies have identified novel biomarkers for type 2 diabetes (T2D) and its complications, such as branched-chain amino acids, metabolites of phenylalanine, metabolites involved in energy metabolism, and lipid metabolism. Metabolomics have also been applied to explore the potential pathways modulated by medications. Investigating diabetes using a systems biology approach by integrating metabolomics with other omics data, such as genetics, transcriptomics, proteomics, and clinical data can present a comprehensive metabolic network and facilitate causal inference. In this regard, metabolomics can deepen the molecular understanding, help identify potential therapeutic targets, and improve the prevention and management of T2D and its complications. The current review focused on metabolomic biomarkers for kidney and cardiovascular disease in T2D identified from epidemiological studies, and will also provide a brief overview on metabolomic investigations for T2D. Full article
(This article belongs to the Special Issue Molecular Mechanisms in Metabolic Disease 2022)
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