El tejido adiposo, ¿solo un almacén de energía? / Adipose Tissue, Just an Energy Storage?

Resumen Cuando los alimentos cubren los requerimientos energéticos, el organismo almacena el exceso de calorías como glucógeno en el hígado y el músculo, y los triacilgliceroles en el tejido adiposo. Morfológica y funcionalmente se clasifica en blanco y pardo. El pardo tiene gran cantidad de mitocondrias, almacena los triacilgliceroles en vacuolas y disipa la energía en forma de calor; el blanco almacena energía en gotas lipídicas que ocupan la mayor parte de su volumen. Después de la ingesta de alimentos se libera insulina, lo que hace que externen GLUT4 para absorber glucosa. Los quilomicrones o las lipoproteínas de muy baja densidad (VLDL) transportan los triacilgliceroles a los depósitos de tejido adiposo. Durante el ayuno, por acción del glucagón, se liberan enzimas que degradarán a los tri, di y monogliceroles para liberar a los ácidos grasos. El tejido adiposo libera citocinas pro y antiinflamatorias, así como leptina, adiponectina que regulan el apetito y la saciedad. La proteína cinasa activada por AMP se activa como respuesta a una baja en la cantidad de energía de la célula y le ayuda a mantener un balance energético. En el adipocito promueve la degradación de los triacilgliceroles para liberar a los ácidos grasos que se emplearán como fuente energética. Se requiere de mayor cantidad de estudios para conocer más sobre la función del tejido adiposo como regulador del metabolismo y no solo como almacén de energía.

Abstract When food meets energy requirements, the body stores in the liver and in the muscle the excess of calories as glycogen and triacylglycerols in the adipose tissue. Morphologically and functionally, it is classified into white and brown tissues. Brown tissue has many large mitochondria and stores triacylglycerols in vacuoles and dissipates energy as heat; white tissue stores energy as lipid droplets that occupy most of the adipocyte's volume. After food intake insulin is released, which causes GLUT4 externalization into the cellular membrane to absorb glucose. Chylomicrons or VLDL transport triacylglycerols to adipose tissue depots. During fasting, by the action of glucagon, enzymes are released that will degrade tri-, di- and mono-glycerols to release fatty acids. Adipose tissue releases pro and anti-inflammatory cytokines, as well as leptin and adiponectin that regulate appetite and satiety. AMPK is activated in response to a decrease in the cell's energy and helps it to maintain its energetic balance. In the adipocyte, it promotes the degradation of triacylglycerols releasing fatty acids to be used as an energy source. More studies are needed to learn more about the function of adipose tissue as a regulator of the metabolism and not only as an energy storage.

The potential mechanisms of white adipose tissue browning: a novel target for the treatment of obesity / Los posibles mecanismos de pardeamiento del tejido adiposo blanco: una diana novedosa para el tratamiento de la obesidad

The increase of the obesity pandemic worldwide over the last several decades has generated a constant need for the scientific world to develop new possibilities to combat obesity. Since the discovery that brown adipose tissue (BAT) exists in adult humans, and BAT activation contributes to a negative energy balance, much more attention has been focused on the understanding of the molecular switches and their different regulatory mechanisms turning on energy expenditure. Recent insights have revealed that a range of stimuli including cold exposure, physical activity and diet, and critical transcription molecules such as PPARγ, PRDM16, PGC-1α and UCP1, aiming at the induction of BAT activation, could cause the browning of white adipose tissue, thereby dissipating energy and increasing heat production. An increasing number of studies that point to the white adipose tissue (WAT) browning strategies aiming at diet-induced and/or genetically determined obesity have been tested in mouse models as well as in human studies. Findings suggested that browning stimulating drugs have been currently or previously assayed as a therapy against obesity. As PPARα agonists, fibrate drugs effectively reduced plasma triglyceride, increased high-density lipoproteins, and improved glycemic control and heat production in brown adipose tissue, which has been used in the treatment of metabolic disorders. Many kinds of natural products promote white adipose tissue browning, such as alkaloids, flavonoids, terpenoids, and long-chain fatty acids, which can also ameliorate metabolic disorders including obesity, insulin resistance and diabetes. The aim of this review is to summarize the transcriptional regulators as well as the various mediators that have been regarded as potential therapeutic targets in the process of WAT browning (AU)

La creciente prevalencia mundial de la obesidad en las últimas décadas ha hecho que la comunidad científica siga necesitando desarrollar nuevas posibilidades para luchar contra la obesidad. Desde que se descubrió que el tejido adiposo pardo (TAP) existe en los adultos y que la activación del TAP contribuye al equilibrio energético negativo, se ha prestado más atención a la comprensión de los interruptores moleculares y sus diferentes mecanismos de regulación del consumo de energía. Estudios recientes han demostrado que una serie de estímulos, incluyendo la exposición al frío, la actividad física y la dieta, y moléculas clave de transcripción como PPARγ, PRDM16, PGC-1α y UCP1, dirigidos a inducir la activación del TAP, podrían causar un pardeamiento del tejido adiposo blanco (TAB), disipando energía y aumentando la producción de calor. Se han realizado un número cada vez mayor de estudios sobre estrategias de pardeamiento del TAB para la obesidad inducida por la dieta y/o genéticamente determinada, tanto en modelos de ratón como en modelos de líneas celulares humanas in vitro. Desafortunadamente, el potencial terapéutico de estas estrategias de pérdida de peso mediante la inducción de la activación del TAP y el pardeamiento del TAB no se ha confirmado en seres humanos. El objetivo de esta revisión es resumir los reguladores de la transcripción y los mediadores que se consideran objetivos terapéuticos potenciales en el proceso de pardeamiento del TAB (AU)

Los posibles mecanismos de pardeamiento del tejido adiposo blanco: una diana novedosa para el tratamiento de la obesidad.

Introduction: The increase of the obesity pandemic worldwide over the last several decades has generated a constant need for the scientific world to develop new possibilities to combat obesity. Since the discovery that brown adipose tissue (BAT) exists in adult humans, and BAT activation contributes to a negative energy balance, much more attention has been focused on the understanding of the molecular switches and their different regulatory mechanisms turning on energy expenditure. Recent insights have revealed that a range of stimuli including cold exposure, physical activity and diet, and critical transcription molecules such as PPARγ, PRDM16, PGC-1α and UCP1, aiming at the induction of BAT activation, could cause the browning of white adipose tissue, thereby dissipating energy and increasing heat production. An increasing number of studies that point to the white adipose tissue (WAT) browning strategies aiming at diet-induced and/or genetically determined obesity have been tested in mouse models as well as in human studies. The aim of this review is to summarize the transcriptional regulators as well as the various mediators that have been regarded as potential therapeutic targets in the process of WAT browning.

Introducción: La creciente prevalencia mundial de la obesidad en las últimas décadas ha hecho que la comunidad científica siga necesitando desarrollar nuevas posibilidades para luchar contra la obesidad. Desde que se descubrió que el tejido adiposo pardo (TAP) existe en los adultos y que la activación del TAP contribuye al equilibrio energético negativo, se ha prestado más atención a la comprensión de los interruptores moleculares y sus diferentes mecanismos de regulación del consumo de energía. Estudios recientes han demostrado que una serie de estímulos, incluyendo la exposición al frío, la actividad física y la dieta, y moléculas clave de transcripción como PPARγ, PRDM16, PGC-1α y UCP1, dirigidos a inducir la activación del TAP, podrían causar un pardeamiento del tejido adiposo blanco (TAB), disipando energía y aumentando la producción de calor. Se ha realizado un número cada vez mayor de estudios sobre estrategias de pardeamiento del TAB para la obesidad inducida por la dieta y/o genéticamente determinada. Desafortunadamente, el potencial terapéutico de estas estrategias de pérdida de peso mediante la inducción de la activación del TAP y el pardeamiento del TAB no se ha confirmado en seres humanos. El objetivo de esta revisión es resumir los reguladores de la transcripción y los mediadores que se consideran objetivos terapéuticos potenciales en el proceso de pardeamiento del TAB.

18F-FDG PET/CT brown fat detection: Differences between adult and pediatric population in a 12 year experience. / Detección de grasa parda en la PET/TC con 18F-FDG: diferencias entre la población adulta y pediátrica en una experiencia de 12 años.

PURPOSE: To analyze epidemiological and anthropometric features of patients with brown adipose tissue (BAT) activation detected by fluorine18-fluorodeoxyglucose positron emission tomography/computed tomography (18F-FDG PET/CT). MATERIAL AND METHODS: From 2005 to 2017, 818 18F-FDG PET/CT studies positive for BAT detection were retrospectively included, 742 examinations performed on the adult population and 76 PET/CT on the pediatric population. A Chi-squared test was performed to compare features distribution between the adult and pediatric patients. RESULTS: Adults showed a higher rate of BAT detection in females (79% vs. 61%, P<0.001) and in hyperglycaemic patients (>100mg/dL) (24% vs. 16%, P=0.02), no significant difference was found with regard to overweight patients (BMI>25kg/m2) (22% vs. 20%, P=.55). Considering females only, the adults showed a higher rate of BAT detection both in hyperglycaemic (83% vs. 42%, P<0.001) and overweight patients (80% vs. 67%, P=0.005). In both populations BAT activation happened more frequently in cold seasons; there was no significant distribution difference with regard to season of birth (P=0.2). CONCLUSIONS: Sex, glycemia and BMI play a major role in predicting BAT activation, with significant differences between adults and pediatric patients. Cold exposure is confirmed as an important predicting factor, while season of birth is not significant.

Hibernomas en cabeza y cuello: reporte de un caso clínico y revisión de la literatura / Head and neck hibernoma: case report and literature review

En el siguiente artículo se presenta un caso clínico de un adolescente de 14 años que consulta por presentar un aumento de volumen supraclavicular derecho y cuyo diagnóstico final realizado mediante estudio histológico luego de exéresis de la masa, concluye ser un hibernoma. Considerando la infrecuencia con la que se presentan este tipo de tumores benignos de los tejidos blandos, presentamos una descripción, mediante revisión bibliográfica, de dicha patología.

In this article, we present a clinical case of a 14 years old teen who presented a su-pracavicular growing mass and whose diagnosis made by histologic examination after performing excision, proves to be a hibernoma. Given the infrequency with wich these types of benign tumors of the soft tissues occur, we present a description, based on a literature review of such pathology.

Extensive hypermetabolic pattern of brown adipose tissue activation on 18F-FDG PET/CT in a patient diagnosed of catecholamine-secreting para-vesical paraganglioma.

The widespread use of (18)F-FDG PET-CT scanning in oncological patients has allowed to demonstrate the existence of metabolically active brown fat, also called brown adipose tissue (BAT), in adult humans, and specifying its anatomical distribution in vivo. As physiological determinants to BAT (18)F-FDG uptake has been identified gender, age, temperature, and body mass index. We have observed extensive activation of the BAT, including the mesenteric region, in a patient with a catecholamine-secreting para-vesical paranganglioma. The extensive BAT activation could be secondary to adrenergic stimulation due to excess of circulating norepinephrine concentration.