Beneficial effects of IKKε-deficiency on body weight and insulin sensitivity are lost in high fat diet-induced obesity in mice.
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Beneficial effects of IKKε-deficiency on body weight and insulin sensitivity are lost in high fat diet-induced obesity in mice. / Scheja, Ludger; Heese, Barbara; Seedorf, Klaus.
in: BIOCHEM BIOPH RES CO, Jahrgang 407, Nr. 2, 2, 2011, S. 288-294.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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TY - JOUR
T1 - Beneficial effects of IKKε-deficiency on body weight and insulin sensitivity are lost in high fat diet-induced obesity in mice.
AU - Scheja, Ludger
AU - Heese, Barbara
AU - Seedorf, Klaus
PY - 2011
Y1 - 2011
N2 - Activation of the classical I?B kinases (IKK? and IKK?) was previously shown to contribute to obesity-induced inflammation and insulin resistance. Using knockout mice, we investigated whether the related isoform IKK? plays a similar metabolic role. IKK?(-/-) mice had reduced body weight, leptin levels, as well as higher insulin sensitivity when kept on chow diet. However, inflammatory parameters, measured in liver, adipose tissue and plasma, were either unaltered or showed a trend toward up-regulation (liver NF-?B activity, TNF? and IL-1? expression). Chronic feeding of a high fat diet induced equal obesity and insulin resistance, and similarly induced inflammatory markers, in IKK?(-/-) and wild-type mice, indicating that under high caloric conditions the inflammatory and metabolic effects of IKK? deficiency were overridden. Taken together, our data indicate that IKK? does not have general pro-inflammatory properties in liver and adipose tissue, and suggest that reduced adiposity is the primary mechanism for improved insulin sensitivity in IKK?(-/-) mice on chow diet.
AB - Activation of the classical I?B kinases (IKK? and IKK?) was previously shown to contribute to obesity-induced inflammation and insulin resistance. Using knockout mice, we investigated whether the related isoform IKK? plays a similar metabolic role. IKK?(-/-) mice had reduced body weight, leptin levels, as well as higher insulin sensitivity when kept on chow diet. However, inflammatory parameters, measured in liver, adipose tissue and plasma, were either unaltered or showed a trend toward up-regulation (liver NF-?B activity, TNF? and IL-1? expression). Chronic feeding of a high fat diet induced equal obesity and insulin resistance, and similarly induced inflammatory markers, in IKK?(-/-) and wild-type mice, indicating that under high caloric conditions the inflammatory and metabolic effects of IKK? deficiency were overridden. Taken together, our data indicate that IKK? does not have general pro-inflammatory properties in liver and adipose tissue, and suggest that reduced adiposity is the primary mechanism for improved insulin sensitivity in IKK?(-/-) mice on chow diet.
KW - Animals
KW - Male
KW - Mice
KW - Mice, Knockout
KW - NF-kappa B/metabolism
KW - Biological Markers/blood
KW - Body Weight/genetics
KW - Dietary Fats/administration & dosage/adverse effects
KW - I-kappa B Kinase/genetics
KW - Inflammation Mediators/blood
KW - Insulin Resistance/genetics
KW - Liver/enzymology
KW - Obesity/blood/enzymology/etiology
KW - Animals
KW - Male
KW - Mice
KW - Mice, Knockout
KW - NF-kappa B/metabolism
KW - Biological Markers/blood
KW - Body Weight/genetics
KW - Dietary Fats/administration & dosage/adverse effects
KW - I-kappa B Kinase/genetics
KW - Inflammation Mediators/blood
KW - Insulin Resistance/genetics
KW - Liver/enzymology
KW - Obesity/blood/enzymology/etiology
M3 - SCORING: Journal article
VL - 407
SP - 288
EP - 294
JO - BIOCHEM BIOPH RES CO
JF - BIOCHEM BIOPH RES CO
SN - 0006-291X
IS - 2
M1 - 2
ER -
