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Vitamin A and feeding statuses modulate the insulin-regulated gene expression in Zucker lean and fatty primary rat hepatocytes.

Chen W, Howell ML, Li Y, Li R, Chen G - PLoS ONE (2014)

Bottom Line: Unattended hepatic insulin resistance predisposes individuals to dyslipidemia, type 2 diabetes and many other metabolic complications.To examine the effects of vitamin A (VA), total energy intake and feeding conditions on the insulin-regulated gene expression in primary hepatocytes of Zucker lean (ZL) and fatty (ZF) rats, we analyze the expression levels of hepatic model genes in response to the treatments of insulin and retinoic acid (RA).These results demonstrate that VA and feeding statuses modulate the hepatic insulin sensitivity at the gene expression level.

View Article: PubMed Central - PubMed

Affiliation: Department of Nutrition, University of Tennessee at Knoxville, Knoxville, Tennessee, United States of America.

ABSTRACT
Unattended hepatic insulin resistance predisposes individuals to dyslipidemia, type 2 diabetes and many other metabolic complications. The mechanism of hepatic insulin resistance at the gene expression level remains unrevealed. To examine the effects of vitamin A (VA), total energy intake and feeding conditions on the insulin-regulated gene expression in primary hepatocytes of Zucker lean (ZL) and fatty (ZF) rats, we analyze the expression levels of hepatic model genes in response to the treatments of insulin and retinoic acid (RA). We report that the insulin- and RA-regulated glucokinase, sterol regulatory element-binding protein-1c and cytosolic form of phosphoenolpyruvate carboxykinase expressions are impaired in hepatocytes of ZF rats fed chow or a VA sufficient (VAS) diet ad libitum. The impairments are partially corrected when ZF rats are fed a VA deficient (VAD) diet ad libitum or pair-fed a VAS diet to the intake of their VAD counterparts in non-fasting conditions. Interestingly in the pair-fed ZL and ZF rats, transient overeating on the last day of pair-feeding regimen changes the expression levels of some VA catabolic genes, and impairs the insulin- and RA-regulated gene expression in hepatocytes. These results demonstrate that VA and feeding statuses modulate the hepatic insulin sensitivity at the gene expression level.

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Insulin-induced Gck expression was attenuated in hepatocytes from VAS-PF-AD, but not VAS-PF-4M rats.The primary hepatocytes were treated by insulin (0 nM to 100 nM) with or without RA (5 µM) in medium A for 6 hours. The expression level of Gck was determined by real-time PCR analysis, and the data were expressed as fold induction. The gene transcript levels from the no treatment group (0 nM insulin, no RA) for both ZL and ZF were arbitrarily set to 1. All p<0.05; for (A), a<b<c, a′<b′<c′, a″<b″<c″, d<e<f, d′<f′/g′, e′<g′, d″<e″<f″; for (B), h<i<j, h′<i′, h″<i″<j″, k<l<m, j′<k′<l′, k″<i″<m″, using one way ANOVA. *, #, and $ for comparing the effects of dietary manipulations at any treatment using one way ANOVA.
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pone-0100868-g005: Insulin-induced Gck expression was attenuated in hepatocytes from VAS-PF-AD, but not VAS-PF-4M rats.The primary hepatocytes were treated by insulin (0 nM to 100 nM) with or without RA (5 µM) in medium A for 6 hours. The expression level of Gck was determined by real-time PCR analysis, and the data were expressed as fold induction. The gene transcript levels from the no treatment group (0 nM insulin, no RA) for both ZL and ZF were arbitrarily set to 1. All p<0.05; for (A), a<b<c, a′<b′<c′, a″<b″<c″, d<e<f, d′<f′/g′, e′<g′, d″<e″<f″; for (B), h<i<j, h′<i′, h″<i″<j″, k<l<m, j′<k′<l′, k″<i″<m″, using one way ANOVA. *, #, and $ for comparing the effects of dietary manipulations at any treatment using one way ANOVA.

Mentions: In ZL hepatocytes, insulin dose-dependently induced the Gck expression (Figure 5A). Without or with RA, the fold inductions by insulin in VAS-PF-AD ZL hepatocytes were significantly lower than that in VAD-AD hepatocytes (marked by *) and VAS-PF-4M ZL hepatocytes (marked by $), suggesting an impaired insulin regulation. Additionally, the fold inductions by insulin in VAD-AD ZL hepatocytes were lower than that of VAS-PF-4M ZL hepatocytes without or with RA (marked by #). These results match the data shown in Figure 2A and indicate that VA status of ZL rats affects the insulin-stimulated Gck expression in their hepatocytes.


Vitamin A and feeding statuses modulate the insulin-regulated gene expression in Zucker lean and fatty primary rat hepatocytes.

Chen W, Howell ML, Li Y, Li R, Chen G - PLoS ONE (2014)

Insulin-induced Gck expression was attenuated in hepatocytes from VAS-PF-AD, but not VAS-PF-4M rats.The primary hepatocytes were treated by insulin (0 nM to 100 nM) with or without RA (5 µM) in medium A for 6 hours. The expression level of Gck was determined by real-time PCR analysis, and the data were expressed as fold induction. The gene transcript levels from the no treatment group (0 nM insulin, no RA) for both ZL and ZF were arbitrarily set to 1. All p<0.05; for (A), a<b<c, a′<b′<c′, a″<b″<c″, d<e<f, d′<f′/g′, e′<g′, d″<e″<f″; for (B), h<i<j, h′<i′, h″<i″<j″, k<l<m, j′<k′<l′, k″<i″<m″, using one way ANOVA. *, #, and $ for comparing the effects of dietary manipulations at any treatment using one way ANOVA.
© Copyright Policy
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4126667&req=5

pone-0100868-g005: Insulin-induced Gck expression was attenuated in hepatocytes from VAS-PF-AD, but not VAS-PF-4M rats.The primary hepatocytes were treated by insulin (0 nM to 100 nM) with or without RA (5 µM) in medium A for 6 hours. The expression level of Gck was determined by real-time PCR analysis, and the data were expressed as fold induction. The gene transcript levels from the no treatment group (0 nM insulin, no RA) for both ZL and ZF were arbitrarily set to 1. All p<0.05; for (A), a<b<c, a′<b′<c′, a″<b″<c″, d<e<f, d′<f′/g′, e′<g′, d″<e″<f″; for (B), h<i<j, h′<i′, h″<i″<j″, k<l<m, j′<k′<l′, k″<i″<m″, using one way ANOVA. *, #, and $ for comparing the effects of dietary manipulations at any treatment using one way ANOVA.
Mentions: In ZL hepatocytes, insulin dose-dependently induced the Gck expression (Figure 5A). Without or with RA, the fold inductions by insulin in VAS-PF-AD ZL hepatocytes were significantly lower than that in VAD-AD hepatocytes (marked by *) and VAS-PF-4M ZL hepatocytes (marked by $), suggesting an impaired insulin regulation. Additionally, the fold inductions by insulin in VAD-AD ZL hepatocytes were lower than that of VAS-PF-4M ZL hepatocytes without or with RA (marked by #). These results match the data shown in Figure 2A and indicate that VA status of ZL rats affects the insulin-stimulated Gck expression in their hepatocytes.

Bottom Line: Unattended hepatic insulin resistance predisposes individuals to dyslipidemia, type 2 diabetes and many other metabolic complications.To examine the effects of vitamin A (VA), total energy intake and feeding conditions on the insulin-regulated gene expression in primary hepatocytes of Zucker lean (ZL) and fatty (ZF) rats, we analyze the expression levels of hepatic model genes in response to the treatments of insulin and retinoic acid (RA).These results demonstrate that VA and feeding statuses modulate the hepatic insulin sensitivity at the gene expression level.

View Article: PubMed Central - PubMed

Affiliation: Department of Nutrition, University of Tennessee at Knoxville, Knoxville, Tennessee, United States of America.

ABSTRACT
Unattended hepatic insulin resistance predisposes individuals to dyslipidemia, type 2 diabetes and many other metabolic complications. The mechanism of hepatic insulin resistance at the gene expression level remains unrevealed. To examine the effects of vitamin A (VA), total energy intake and feeding conditions on the insulin-regulated gene expression in primary hepatocytes of Zucker lean (ZL) and fatty (ZF) rats, we analyze the expression levels of hepatic model genes in response to the treatments of insulin and retinoic acid (RA). We report that the insulin- and RA-regulated glucokinase, sterol regulatory element-binding protein-1c and cytosolic form of phosphoenolpyruvate carboxykinase expressions are impaired in hepatocytes of ZF rats fed chow or a VA sufficient (VAS) diet ad libitum. The impairments are partially corrected when ZF rats are fed a VA deficient (VAD) diet ad libitum or pair-fed a VAS diet to the intake of their VAD counterparts in non-fasting conditions. Interestingly in the pair-fed ZL and ZF rats, transient overeating on the last day of pair-feeding regimen changes the expression levels of some VA catabolic genes, and impairs the insulin- and RA-regulated gene expression in hepatocytes. These results demonstrate that VA and feeding statuses modulate the hepatic insulin sensitivity at the gene expression level.

Show MeSH
Related in: MedlinePlus