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      La tormentosa relación entre las grasas y el desarrollo de la diabetes mellitus tipo 2: actualizado. Parte 2 Translated title: The stormy relationship between fats and the development of type 2 diabetes mellitus: Updated. Part 2

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          Abstract

          En esta parte de la revisión se describe la relación funcional entre el metabolismo de los lípidos y los hidratos de carbono y su interdependencia, desde el ciclo glucosa-ácido grasos y la hipótesis portal de la insulinorresistencia a los nuevos conocimientos sobre los adipocitos marrones y beiges, con énfasis en el normal funcionamiento de un patrón endocrino cuya disfunción es clave en la fisiopatología de la DMT2 y la obesidad. Se discute la ectopia o el asiento de grasa en el tejido magro por incapacidad del tejido adiposo para seguir acopiando lípidos y la actividad endocrina del adipocito, con la producción de moléculas (adipoquinas) que influyen sobre los mecanismos inductores de insulinorresistencia (leptina, adiponectina, TNF-α, resistina, etc.) y disfunción de la célula beta. Se describen la disminución de la capacidad oxidativa en la cadena respiratoria mitocondrial y el renacer del concepto de lipogénesis de novo, ambas favoreciendo el acopie de lípido intracelular. En tejidos magros existen pequeñas reservas intracelulares de lípidos que mantienen la regulación de funciones esenciales, aunque si aparece una sobrecarga lipídica el fenómeno conduciría a una disfunción (lipotoxicidad) y a la muerte celular (lipoapoptosis). La tormentosa relación entre los lípidos y el islote de Langerhans va más allá del esfuerzo funcional que impone la insulinorresistencia periférica sobre la célula β, por efectos directos de los lípidos o de sus derivados sobre la función del islote pancreático. Sin déficit de insulina no se desarrolla diabetes.

          Translated abstract

          In this part of the review, the functional relationship between lipid and carbohydrate metabolisms and their interdependence is described, from the glucose-fatty acid cycle and the portal hypothesis of insulin resistance to the new knowledge on brown and beige adipocytes, with emphasis on the normal functioning of an endocrine pattern in which its dysfunction is a key factor in the pathophysiology of T2DM and obesity. Ectopic fat deposition in lean tissues due to the inability of the adipose tissue to continuously collect lipids and the endocrine activity of adipocytes is discussed. The production of molecules (adipokines) influencing some of the mechanisms involved in the development of insulin resistance (leptin, adiponectin, TNF-α, resistin, etc.) and beta cell dysfunction is also revisited. The decrease in the oxidative capacity in the mitochondrial respiratory chain and the rebirth of the concept of de novo lipogenesis are described, both effects favouring intracellular lipid accumulation. In lean tissues there are small intracellular lipid reserves that help to maintain the regulation of essential functions; however, when a lipid overload occurs the phenomenon could lead to severe cell dysfunction (lipotoxicity), and death (lipo-apoptosis). The stormy relationship between lipids and the Langerhans' islets goes beyond the functional effort imposed by peripheral insulin-resistance on the β cells, either by the direct effect of lipids or by their derivatives on overall pancreatic islet function. Within a scenario of no insulin deficit, diabetes does not develop.

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          Most cited references 148

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          Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance

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            A cold-inducible coactivator of nuclear receptors linked to adaptive thermogenesis.

            Adaptive thermogenesis is an important component of energy homeostasis and a metabolic defense against obesity. We have cloned a novel transcriptional coactivator of nuclear receptors, termed PGC-1, from a brown fat cDNA library. PGC-1 mRNA expression is dramatically elevated upon cold exposure of mice in both brown fat and skeletal muscle, key thermogenic tissues. PGC-1 greatly increases the transcriptional activity of PPARgamma and the thyroid hormone receptor on the uncoupling protein (UCP-1) promoter. Ectopic expression of PGC-1 in white adipose cells activates expression of UCP-1 and key mitochondrial enzymes of the respiratory chain, and increases the cellular content of mitochondrial DNA. These results indicate that PGC-1 plays a key role in linking nuclear receptors to the transcriptional program of adaptive thermogenesis.
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              PRDM16 controls a brown fat/skeletal muscle switch.

              Brown fat can increase energy expenditure and protect against obesity through a specialized program of uncoupled respiration. Here we show by in vivo fate mapping that brown, but not white, fat cells arise from precursors that express Myf5, a gene previously thought to be expressed only in the myogenic lineage. We also demonstrate that the transcriptional regulator PRDM16 (PRD1-BF1-RIZ1 homologous domain containing 16) controls a bidirectional cell fate switch between skeletal myoblasts and brown fat cells. Loss of PRDM16 from brown fat precursors causes a loss of brown fat characteristics and promotes muscle differentiation. Conversely, ectopic expression of PRDM16 in myoblasts induces their differentiation into brown fat cells. PRDM16 stimulates brown adipogenesis by binding to PPAR-gamma (peroxisome-proliferator-activated receptor-gamma) and activating its transcriptional function. Finally, Prdm16-deficient brown fat displays an abnormal morphology, reduced thermogenic gene expression and elevated expression of muscle-specific genes. Taken together, these data indicate that PRDM16 specifies the brown fat lineage from a progenitor that expresses myoblast markers and is not involved in white adipogenesis.
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                Author and article information

                Contributors
                Role: ND
                Role: ND
                Journal
                raem
                Revista argentina de endocrinología y metabolismo
                Rev. argent. endocrinol. metab.
                Sociedad Argentina de Endocrinología y Metabolismo (Ciudad Autónoma de Buenos Aires, , Argentina )
                1851-3034
                December 2017
                : 54
                : 4
                : 185-195
                Affiliations
                La Plata Buenos Aires orgnameUNLP-CONICET-FCM orgdiv1CENEXA Argentina
                CABA orgnameUniversidad Favaloro Argentina
                Article
                S1851-30342017000400006
                10.1016/j.raem.2017.06.001

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

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                Figures: 0, Tables: 0, Equations: 0, References: 52, Pages: 11
                Product
                Product Information: SciELO Argentina

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