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Metabolites
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Insulin Resistance, Adipose Tissue Metabolism and Type 2 Diabetes
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Insulin Resistance, Adipose Tissue Metabolism and Type 2 Diabetes

A special issue of Metabolites (ISSN 2218-1989). This special issue belongs to the section "Endocrinology and Clinical Metabolic Research".

Deadline for manuscript submissions: closed (30 June 2022) | Viewed by 9017

Special Issue Editor

Prof. Dr. Maria João Pereira

E-Mail Website
Guest Editor
Department of Medical Sciences, Clinical Diabetes and Metabolism, Uppsala University, 751 85 Uppsala, Sweden
Interests: metabolism; insulin resistance; diabetes; adipose tissue; adipocytes; inflammation; pharmacological therapy; neuroendocrine
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Previously considered to be a passive depot for lipid storage, adipose tissue is nowadays considered a major active endocrine organ, capable of secreting several factors responsive to systemic metabolic changes, and can rapidly and dynamically respond to alterations in nutrient supply and neuroendocrine communication with many other organs. With the rise of obesity, and due to much elegant scientific research, it has become clear that dysfunctional adipose tissue plays a pivotal role in the development of insulin resistance and type 2 diabetes.

This Special Issue aims to feature insights into adipose tissue mechanisms involved in the development of insulin resistance and type 2 diabetes, since a better understanding of these mechanisms could provide new strategies for effective prevention, diagnostics, and treatment. The topics that this Special Issue will cover (not exclusively) include: adipose tissue crosstalk with other tissues/organs such as the brain, immunometabolism, neuroendocrine mechanisms, adipocyte-immune cell crosstalk, adipose tissue immune-cellular composition, hypoxia, browning, mitochondria function, and glucose and the lipid metabolism. Studies may also use interventions, such as bariatric surgery or pharmacological treatment and -omics approaches.

Dr. Maria João Pereira
Guest Editor

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. Metabolites is an international peer-reviewed open access monthly 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

  • adipose tissue
  • insulin resistance
  • metabolism
  • obesity
  • adipocyte
  • crosstalk
  • immunometabolism
  • neuroendocrine
  • inflammation
  • signaling

Published Papers (4 papers)

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Research

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16 pages, 2111 KiB  
Article
Several Metabolite Families Display Inflexibility during Glucose Challenge in Patients with Type 2 Diabetes: An Untargeted Metabolomics Study
by Giovanni Fanni, Jan W. Eriksson and Maria J. Pereira
Metabolites 2023, 13(1), 131; https://doi.org/10.3390/metabo13010131 - 15 Jan 2023
Viewed by 2330
Abstract
Metabolic inflexibility is a hallmark of insulin resistance and can be extensively explored with high-throughput metabolomics techniques. However, the dynamic regulation of the metabolome during an oral glucose tolerance test (OGTT) in subjects with type 2 diabetes (T2D) is largely unknown. We aimed [...] Read more.
Metabolic inflexibility is a hallmark of insulin resistance and can be extensively explored with high-throughput metabolomics techniques. However, the dynamic regulation of the metabolome during an oral glucose tolerance test (OGTT) in subjects with type 2 diabetes (T2D) is largely unknown. We aimed to identify alterations in metabolite responses to OGTT in subjects with T2D using untargeted metabolomics of both plasma and subcutaneous adipose tissue (SAT) samples. Twenty subjects with T2D and twenty healthy controls matched for sex, age, and body mass index (BMI) were profiled with untargeted metabolomics both in plasma (755 metabolites) and in the SAT (588) during an OGTT. We assessed metabolite concentration changes 90 min after the glucose load, and those responses were compared between patients with T2D and controls. Post-hoc analyses were performed to explore the associations between glucose-induced metabolite responses and markers of obesity and glucose metabolism, sex, and age. During the OGTT, T2D subjects had an impaired reduction in plasma levels of several metabolite families, including acylcarnitines, amino acids, acyl ethanolamines, and fatty acid derivates (p < 0.05), compared to controls. Additionally, patients with T2D had a greater increase in plasma glucose and fructose levels during the OGTT compared to controls (p < 0.05). The plasma concentration change of most metabolites after the glucose load was mainly associated with indices of hyperglycemia rather than insulin resistance, insulin secretion, or BMI. In multiple linear regression analyses, hyperglycemia indices (glucose area under the curve (AUC) during OGTT and glycosylated hemoglobin (HbA1c)) were the strongest predictors of plasma metabolite changes during the OGTT. No differences were found in the adipose tissue metabolome in response to the glucose challenge between T2D and controls. Using a metabolomics approach, we show that T2D patients display attenuated responses in several circulating metabolite families during an OGTT. Besides the well-known increase in monosaccharides, the glucose-induced lowering of amino acids, acylcarnitines, and fatty acid derivatives was attenuated in T2D subjects compared to controls. These data support the hypothesis of inflexibility in several metabolic pathways, which may contribute to dysregulated substrate partitioning and turnover in T2D. These findings are not directly associated with changes in adipose tissue metabolism; therefore, other tissues, such as muscle and liver, are probably of greater importance. Full article
(This article belongs to the Special Issue Insulin Resistance, Adipose Tissue Metabolism and Type 2 Diabetes)
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16 pages, 2970 KiB  
Article
PET/MRI-Evaluated Activation of Brown Adipose Tissue via Cold Exposure Impacts Lipid Metabolism
by Katarzyna Miniewska, Katarzyna Maliszewska, Karolina Pietrowska, Joanna Godzień, Łukasz Łabieniec, Małgorzata Mojsak, Adam Krętowski and Michał Ciborowski
Metabolites 2022, 12(5), 456; https://doi.org/10.3390/metabo12050456 - 19 May 2022
Cited by 2 | Viewed by 2289
Abstract
Although brown adipose tissue (BAT) is considered to play a protective role against obesity and type 2 diabetes, the mechanisms of its activation and associations with clinical parameters are not well described. Male adults underwent a 2 h cold exposure (CE) to activate [...] Read more.
Although brown adipose tissue (BAT) is considered to play a protective role against obesity and type 2 diabetes, the mechanisms of its activation and associations with clinical parameters are not well described. Male adults underwent a 2 h cold exposure (CE) to activate BAT and, based on the results of PET/MRI performed after the CE, were divided into BAT(+) and BAT(−) groups. During the CE procedure, blood samples were collected and alterations in plasma metabolome in both groups were investigated using LC-MS. Additionally, associations between clinical factors and BAT were examined. Moreover, levels of glucose, insulin, leptin, TNF-α, FGF21, and FABP4 were assessed in serum samples. In the BAT(+) group, levels of LPC(17:0), LPE(20:4), LPE(22:4), LPE(22:6), DHA, linoleic acid, and oleic acid increased during CE, whereas levels of sphinganine-phosphate and sphingosine-1-phosphate decreased. Levels of LPE(O-18:0), 9-HpODE, and oleic acid were elevated, while the level of LPE(20:5) was reduced in BAT(+) compared to BAT(−) subjects. AUCs of LPC(18:2), LPC(O-18:2)/LPC(P-18:1), and SM(d32:2) negatively correlated with BAT. In the BAT(+) group, the concentration of FABP4 during and after CE was decreased compared to the basal level. No alterations were observed in the BAT(−) group. In conclusion, using untargeted metabolomics, we proved that the plasma metabolome is affected by cold-induced BAT activation. Full article
(This article belongs to the Special Issue Insulin Resistance, Adipose Tissue Metabolism and Type 2 Diabetes)
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10 pages, 685 KiB  
Article
Plasma Tsukushi Concentration Is Associated with High Levels of Insulin and FGF21 and Low Level of Total Cholesterol in a General Population without Medication
by Masato Furuhashi, Yukimura Higashiura, Akiko Sakai, Masayuki Koyama, Marenao Tanaka, Shigeyuki Saitoh, Kazuaki Shimamoto and Hirofumi Ohnishi
Metabolites 2022, 12(3), 237; https://doi.org/10.3390/metabo12030237 - 10 Mar 2022
Cited by 2 | Viewed by 2055
Abstract
Tsukushi (TSK) is a member of the small leucine-rich proteoglycan family that controls developmental processes and organogenesis. TSK was also identified as a new hepatokine, which is mainly expressed in the liver, and is secreted by hepatocytes, to regulate energy and glycolipid metabolism [...] Read more.
Tsukushi (TSK) is a member of the small leucine-rich proteoglycan family that controls developmental processes and organogenesis. TSK was also identified as a new hepatokine, which is mainly expressed in the liver, and is secreted by hepatocytes, to regulate energy and glycolipid metabolism in response to nonalcoholic fatty liver disease. However, the role of plasma TSK, especially its role in the general population, has not been fully addressed. We investigated the associations between plasma TSK concentration and several metabolic markers, including fibroblast growth factor 21 (FGF21), a hepatokine, and adiponectin, an adipokine, in 253 subjects (men/women: 114/139) with no medication in the Tanno–Sobetsu Study, which employed a population-based cohort. There was no significant sex difference in plasma TSK concentration, and the level was positively correlated with the fatty liver index (FLI) (r = 0.131, p = 0.038), levels of insulin (r = 0.295, p < 0.001) and levels of FGF21 (r = 0.290, p < 0.001), and was negatively correlated with the total cholesterol level (r = −0.124, p = 0.049). There was no significant correlation between the TSK level and body mass index, waist circumference, adiponectin, high-density lipoprotein cholesterol or total bile acids. The multivariable regression analysis showed that high levels of insulin and FGF21 and a low level of total cholesterol were independent determinants of plasma TSK concentration, after adjustment for age, sex and FLI. In conclusion, plasma TSK concentration is independently associated with high levels of insulin and FGF21, a hepatokine, and a low level of total cholesterol, but not with adiposity and adiponectin, in a general population of subjects who have not taken any medications. Full article
(This article belongs to the Special Issue Insulin Resistance, Adipose Tissue Metabolism and Type 2 Diabetes)
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Review

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21 pages, 763 KiB  
Review
Galectin-1 in Obesity and Type 2 Diabetes
by Emanuel Fryk, Vagner R. R. Silva and Per-Anders Jansson
Metabolites 2022, 12(10), 930; https://doi.org/10.3390/metabo12100930 - 30 Sep 2022
Cited by 8 | Viewed by 1848
Abstract
Galectin-1 is a carbohydrate-binding protein expressed in many tissues. In recent years, increasing evidence has emerged for the role of galectin-1 in obesity, insulin resistance and type 2 diabetes. Galectin-1 has been highly conserved through evolution and is involved in key cellular functions [...] Read more.
Galectin-1 is a carbohydrate-binding protein expressed in many tissues. In recent years, increasing evidence has emerged for the role of galectin-1 in obesity, insulin resistance and type 2 diabetes. Galectin-1 has been highly conserved through evolution and is involved in key cellular functions such as tissue maturation and homeostasis. It has been shown that galectin-1 increases in obesity, both in the circulation and in the adipose tissue of human and animal models. Several proteomic studies have independently identified an increased galectin-1 expression in the adipose tissue in obesity and in insulin resistance. Large population-based cohorts have demonstrated associations for circulating galectin-1 and markers of insulin resistance and incident type 2 diabetes. Furthermore, galectin-1 is associated with key metabolic pathways including glucose and lipid metabolism, as well as insulin signalling and inflammation. Intervention studies in animal models alter animal weight and metabolic profile. Several studies have also linked galectin-1 to the progression of complications in diabetes, including kidney disease and retinopathy. Here, we review the current knowledge on the clinical potential of galectin-1 in obesity and type 2 diabetes. Full article
(This article belongs to the Special Issue Insulin Resistance, Adipose Tissue Metabolism and Type 2 Diabetes)
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