2011
DOI: 10.1038/labinvest.2011.6
|View full text |Cite
|
Sign up to set email alerts
|

Carnitine is necessary to maintain the phenotype and function of brown adipose tissue

Abstract: The juvenile visceral steatosis (JVS) mouse is a mutant strain with an inherited systemic carnitine deficiency. Mice of this strain show clinical signs attributable to impaired heat production and disturbed energy production. Brown adipose tissue (BAT) is the primary site of non-shivering thermogenesis in the presence of uncoupling protein-1 (UCP-1) in rodents and humans, especially in infants. To investigate the possible cause of impaired heat production in BAT, we studied the morphological features, carnitin… Show more

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...
2
1
1
1

Citation Types

6
15
0

Year Published

2013
2013
2024
2024

Publication Types

Select...
6
2

Relationship

0
8

Authors

Journals

citations
Cited by 22 publications
(21 citation statements)
references
References 34 publications
6
15
0
Order By: Relevance
“…The fact that ACSL1 A−/− mice are cold intolerant but still retain thermogenic gene induction suggests the defect in CPT2 A−/− BAT gene expression lies between the activation of fatty acids and their oxidation (Ellis et al, 2010). Similar to CPT2 A−/− mice, systemic carnitine deficiency also results in a suppression of Ucp1 expression in BAT (Ozaki et al, 2011). These data suggest that an accumulation of fatty acid metabolites, such as long chain acyl-CoAs for example, may be critical nuclear hormone ligands acting as negative metabolic feedback sensors to link metabolic capacity to nuclear encoded mitochondrial gene expression.…”
Section: Discussionmentioning
confidence: 99%
“…The fact that ACSL1 A−/− mice are cold intolerant but still retain thermogenic gene induction suggests the defect in CPT2 A−/− BAT gene expression lies between the activation of fatty acids and their oxidation (Ellis et al, 2010). Similar to CPT2 A−/− mice, systemic carnitine deficiency also results in a suppression of Ucp1 expression in BAT (Ozaki et al, 2011). These data suggest that an accumulation of fatty acid metabolites, such as long chain acyl-CoAs for example, may be critical nuclear hormone ligands acting as negative metabolic feedback sensors to link metabolic capacity to nuclear encoded mitochondrial gene expression.…”
Section: Discussionmentioning
confidence: 99%
“…It is currently unknown if this pathway played any role in helping maintain the thermogenic capacity of BAT-specific CGI-58 or ATGL knockout mice. Administration of carnitine itself was shown to significantly restore body temperature and BAT morphology in mice with juvenile visceral steatosis [38]. A creatine-driven substrate cycle was recently shown to enhance energy expenditure and thermogenesis in beige and brown adipocytes [27].…”
Section: Thermogenic Fuels In the Absence Of Bat Ld Lipolysismentioning
confidence: 99%
“…Retinoic acid delivery also triggers WAT remodeling, and is accompanied by changes in both muscle-and liver-type CPT1 in adipose tissue (24). Furthermore, decreased CPT1 activity is observed in BAT mitochondria of streptozotocindiabetic mice (14), and carnitine is necessary to maintain the phenotype and function of BAT (33). In this context, CPT1 appears to be an important and necessary component of brown adipocytes, including the brown fat cells appearing in white fat depots.…”
Section: Bmp7 Increases Mitochondrial Activity In Brown Fatmentioning
confidence: 99%