AHR in energy balance regulation

Tutkimustuotos: ArtikkelijulkaisuKatsausartikkeliTieteellinenvertaisarvioitu

Kuvaus

Recent studies on mice genetically modified at the Ahr locus
and fed on high-fat diet have revealed a novel physiological
role for the AHR in energy balance. Globally impaired function
of the receptor counteracts the development of obesity by
increasing energy expenditure, which appears to occur mostly
in the skeletal muscle and brown adipose tissue. On the other
hand, global and tissue-specific loss of AHR signaling can
have opposite effects on liver fat content and their impact on
insulin sensitivity is also context-dependent. As tryptophan
metabolites are key AHR activators, these findings suggest
that the AHR may act as a protein sensor enabling adequate
protein intake from low-protein diets by allowing calorie overfeeding
without resultant obesity.
Alkuperäiskielienglanti
LehtiCurrent opinion in toxicology
Vuosikerta2
Sivut8-14
Sivumäärä7
ISSN2468-2020
DOI - pysyväislinkit
TilaJulkaistu - helmikuuta 2017
OKM-julkaisutyyppiA2 Katsausartikkeli tieteellisessä aikakauslehdessä

Tieteenalat

  • 3111 Biolääketieteet

Lainaa tätä

Pohjanvirta, Raimo. / AHR in energy balance regulation. Julkaisussa: Current opinion in toxicology. 2017 ; Vuosikerta 2. Sivut 8-14.
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title = "AHR in energy balance regulation",
abstract = "Recent studies on mice genetically modified at the Ahr locusand fed on high-fat diet have revealed a novel physiologicalrole for the AHR in energy balance. Globally impaired functionof the receptor counteracts the development of obesity byincreasing energy expenditure, which appears to occur mostlyin the skeletal muscle and brown adipose tissue. On the otherhand, global and tissue-specific loss of AHR signaling canhave opposite effects on liver fat content and their impact oninsulin sensitivity is also context-dependent. As tryptophanmetabolites are key AHR activators, these findings suggestthat the AHR may act as a protein sensor enabling adequateprotein intake from low-protein diets by allowing calorie overfeedingwithout resultant obesity.",
keywords = "3111 Biomedicine, AH RECEPTOR, Energy balance, Brown adipose tissue, White adipose tissue, Diet-induced obesity, HIGH-FAT DIET, Knockout mice, GLUCOSE TOLERANCE, INSULIN SENSITIVITY, TRYPTOPHAN, OBESITY",
author = "Raimo Pohjanvirta",
year = "2017",
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doi = "10.1016/j.cotox.2017.01.002",
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AHR in energy balance regulation. / Pohjanvirta, Raimo.

julkaisussa: Current opinion in toxicology, Vuosikerta 2, 02.2017, s. 8-14.

Tutkimustuotos: ArtikkelijulkaisuKatsausartikkeliTieteellinenvertaisarvioitu

TY - JOUR

T1 - AHR in energy balance regulation

AU - Pohjanvirta, Raimo

PY - 2017/2

Y1 - 2017/2

N2 - Recent studies on mice genetically modified at the Ahr locusand fed on high-fat diet have revealed a novel physiologicalrole for the AHR in energy balance. Globally impaired functionof the receptor counteracts the development of obesity byincreasing energy expenditure, which appears to occur mostlyin the skeletal muscle and brown adipose tissue. On the otherhand, global and tissue-specific loss of AHR signaling canhave opposite effects on liver fat content and their impact oninsulin sensitivity is also context-dependent. As tryptophanmetabolites are key AHR activators, these findings suggestthat the AHR may act as a protein sensor enabling adequateprotein intake from low-protein diets by allowing calorie overfeedingwithout resultant obesity.

AB - Recent studies on mice genetically modified at the Ahr locusand fed on high-fat diet have revealed a novel physiologicalrole for the AHR in energy balance. Globally impaired functionof the receptor counteracts the development of obesity byincreasing energy expenditure, which appears to occur mostlyin the skeletal muscle and brown adipose tissue. On the otherhand, global and tissue-specific loss of AHR signaling canhave opposite effects on liver fat content and their impact oninsulin sensitivity is also context-dependent. As tryptophanmetabolites are key AHR activators, these findings suggestthat the AHR may act as a protein sensor enabling adequateprotein intake from low-protein diets by allowing calorie overfeedingwithout resultant obesity.

KW - 3111 Biomedicine

KW - AH RECEPTOR

KW - Energy balance

KW - Brown adipose tissue

KW - White adipose tissue

KW - Diet-induced obesity

KW - HIGH-FAT DIET

KW - Knockout mice

KW - GLUCOSE TOLERANCE

KW - INSULIN SENSITIVITY

KW - TRYPTOPHAN

KW - OBESITY

U2 - 10.1016/j.cotox.2017.01.002

DO - 10.1016/j.cotox.2017.01.002

M3 - Review Article

VL - 2

SP - 8

EP - 14

JO - Current opinion in toxicology

JF - Current opinion in toxicology

SN - 2468-2020

ER -