WANG, Lihua; LIU, Yiran; HU, Feng    ZHOU, Zhongyu. The potential mechanisms of white adipose tissue browning: a novel target for the treatment of obesity. []. , 39, 2, pp.411-424.   09--2022. ISSN 1699-5198.  https://dx.doi.org/10.20960/nh.03852.

^a

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.

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.

: .

        · | |     · |     · ( pdf )