A collaborative work involving two Adipoplast laboratories reports the discovery of a new mechanism for regulating the metabolism of brown adipose tissue through the hormonal system kallikrein-kinin system.

Home Sin categoría A collaborative work involving two Adipoplast laboratories reports the discovery of a new mechanism for regulating the metabolism of brown adipose tissue through the hormonal system kallikrein-kinin system.

A collaborative work involving two Adipoplast laboratories reports the discovery of a new mechanism for regulating the metabolism of brown adipose tissue through the hormonal system kallikrein-kinin system.

By Adipoplast | Sin categoría | Comments are Closed | 4 May, 2020 | 0

That system, in which bradykinin is a main actor, has been traditionally associated with the physiology of the renal and cardiovascular systems and processes of inflammation and pain. Researchers report the kallikrein-kinin system acts as mechanism of molecular self-control of brown and beige adipose tissue thermogenic activation, and could help prevent the harmful effects of excessive activation of brown adipose tissue occurring in some pathological conditions such as cachexia or recovery from severe burns. The full article is accessible at: https://rdcu.be/b3Ud4Zona de los archivos adjuntos

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Seoane-Collazo P, Liñares-Pose L, Rial-Pensado E, Romero-Picó A, Moreno-Navarrete JM,
Martínez-Sánchez N, Garrido-Gil P, Iglesias-Rey R, Morgan DA, Tomasini N, Malone SA, Senra A, Folgueira C, Medina-Gomez G, Sobrino T, Labandeira-García JL, Nogueiras R, Domingos AI, Fernández-Real JM, Rahmouni K, Diéguez C, López M.

Central nicotine induces browning through hypothalamic κ opioid receptor.

Nat Commun. 2019 Sep 6;10(1):4037. doi: 10.1038/s41467-019-12004-z.

Increased body weight is a major factor that interferes with smoking cessation. Nicotine, the main bioactive compound in tobacco, has been demonstrated to have an impact on energy balance, since it affects both feeding and energy expenditure at the central level. Among the central actions of nicotine on body weight, much attention has been focused on its effect on brown adipose tissue (BAT) thermogenesis, though its effect on browning of white adipose tissue (WAT) is unclear. Here, we show that nicotine induces the browning of WAT through a central mechanism and that this effect is dependent on the κ opioid receptor (KOR), specifically in the lateral hypothalamic area (LHA). Consistent with these findings, smokers show higher levels of uncoupling protein 1 (UCP1) expression in WAT, which correlates with smoking status. These data demonstrate that central nicotine-induced modulation of WAT browning may be a target against human obesity.