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      Association of uncoupling protein ( Ucp) gene polymorphisms with cardiometabolic diseases

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          Abstract

          The hereditary aspect of obesity is a major focus of modern medical genetics. The genetic background is known to determine a higher-than-average prevalence of obesity in certain regions, like Oceania. There is evidence that dysfunction of brown adipose tissue (BAT) may be a risk factor for obesity and type 2 diabetes (T2D). A significant number of studies in the field focus on the UCP family. The Ucp genes code for electron transport carriers. UCP1 (thermogenin) is the most abundant protein of the UCP superfamily and is expressed in BAT, contributing to its capability of generating heat. Single nucleotide polymorphisms (SNPs) of Ucp1–Ucp3 were recently associated with risk of cardiometabolic diseases. This review covers the main Ucp SNPs A–3826G, A–1766G, A–112C, Met229Leu, Ala64Thr ( Ucp1), Ala55Val, G–866A ( Ucp2), and C–55 T ( Ucp3), which may be associated with the development of obesity, disturbance in lipid metabolism, T2D, and cardiovascular diseases.

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          Transcriptional control of brown fat determination by PRDM16.

          Patrick Seale, Shingo Kajimura, Wenli Yang … (2007)
          Brown fat cells are specialized to dissipate energy and can counteract obesity; however, the transcriptional basis of their determination is largely unknown. We show here that the zinc-finger protein PRDM16 is highly enriched in brown fat cells compared to white fat cells. When expressed in white fat cell progenitors, PRDM16 activates a robust brown fat phenotype including induction of PGC-1alpha, UCP1, and type 2 deiodinase (Dio2) expression and a remarkable increase in uncoupled respiration. Transgenic expression of PRDM16 at physiological levels in white fat depots stimulates the formation of brown fat cells. Depletion of PRDM16 through shRNA expression in brown fat cells causes a near total loss of the brown characteristics. PRDM16 activates brown fat cell identity at least in part by simultaneously activating PGC-1alpha and PGC-1beta through direct protein binding. These data indicate that PRDM16 can control the determination of brown fat fate.
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            Complementary action of the PGC-1 coactivators in mitochondrial biogenesis and brown fat differentiation.

            Marc Uldry, Wenli Yang, Julie St-Pierre … (2006)
            Mitochondria play an essential role in the ability of brown fat to generate heat, and the PGC-1 coactivators control several aspects of mitochondrial biogenesis. To investigate their specific roles in brown fat cells, we generated immortal preadipocyte lines from the brown adipose tissue of mice lacking PGC-1alpha. We could then efficiently knockdown PGC-1beta expression by shRNA expression. Loss of PGC-1alpha did not alter brown fat differentiation but severely reduced the induction of thermogenic genes. Cells deficient in either PGC-1alpha or PGC-1beta coactivators showed a small decrease in the differentiation-dependant program of mitochondrial biogenesis and respiration; however, this increase in mitochondrial number and function was totally abolished during brown fat differentiation when both PGC-1alpha and PGC-1beta were deficient. These data show that PGC-1alpha is essential for brown fat thermogenesis but not brown fat differentiation, and the PGC-1 coactivators play an absolutely essential but complementary function in differentiation-induced mitochondrial biogenesis.
            Article 0 comments Cited 195 times – based on 0 reviews     Review now
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              An adoption study of human obesity.

              A Stunkard, T. I. Sørensen, C Hanis … (1986)
              We examined the contributions of genetic factors and the family environment to human fatness in a sample of 540 adult Danish adoptees who were selected from a population of 3580 and divided into four weight classes: thin, median weight, overweight, and obese. There was a strong relation between the weight class of the adoptees and the body-mass index of their biologic parents - for the mothers, P less than 0.0001; for the fathers, P less than 0.02. There was no relation between the weight class of the adoptees and the body-mass index of their adoptive parents. Cumulative distributions of the body-mass index of parents showed similar results; there was a strong relation between the body-mass index of biologic parents and adoptee weight class and no relation between the index of adoptive parents and adoptee weight class. Furthermore, the relation between biologic parents and adoptees was not confined to the obesity weight class, but was present across the whole range of body fatness - from very thin to very fat. We conclude that genetic influences have an important role in determining human fatness in adults, whereas the family environment alone has no apparent effect.
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                Author and article information

                Contributors
                Anna E. Pravednikova: pravednikova.anya@yandex.ru
                Sergey Y. Shevchenko: simurg87@list.ru
                Victor V. Kerchev: vi_dok@citydom.ru
                Manana R. Skhirtladze: lagerind.igb.ras@gmail.com
                Svetlana N. Larina: snlarina07@yandex.ru
                Zaur M. Kachaev: k-z-m@mail.ru
                Alexander D. Egorov: egorov.alek@gmail.com
                Yulii V. Shidlovskii:
                ORCID: http://orcid.org/0000-0002-3643-9889
                yul.biogen@gmail.com
                Journal
                Journal ID (nlm-ta): Mol Med
                Journal ID (iso-abbrev): Mol. Med
                Title: Molecular Medicine
                Publisher: BioMed Central (London )
                ISSN (Print): 1076-1551
                ISSN (Electronic): 1528-3658
                Publication date (Electronic): 25 May 2020
                Publication date PMC-release: 25 May 2020
                Publication date Collection: 2020
                Volume: 26
                Electronic Location Identifier: 51
                Affiliations
                [1 ]GRID grid.419021.f, ISNI 0000 0004 0380 8267, Laboratory of Gene Expression Regulation in Development, , Institute of Gene Biology, Russian Academy of Sciences, ; Moscow, Russia
                [2 ]I.M. Sechenov First Moscow State Medical University, Ministry of Health of the Russian Federation, Moscow, Russia
                Author information
                http://orcid.org/0000-0002-3643-9889
                Article
                Publisher ID: 180
                DOI: 10.1186/s10020-020-00180-4
                PMC ID: 7249395
                PubMed ID: 32450815
                SO-VID: 3095ae57-97ca-4d4a-851a-cc8a14496234
                Copyright © © The Author(s) 2020
                License:

                Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                Date received : 14 January 2020
                Date accepted : 11 May 2020
                Funding
                Funded by: FundRef http://dx.doi.org/10.13039/501100002261, Российский Фонд Фундаментальных Исследований (РФФИ);
                Award ID: 18-34-20065
                Award Recipient :
                Categories
                Subject: Review
                Custom metadata
                issue-copyright-statement © The Author(s) 2020

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