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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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The food intake, body mass and cumulative feed efficiency over 56 days of dietary manipulation.(A) Two-day food intake of ZL and ZF on VAD ad libitum (VAD-AD, n = 5), VAS-Pair-feeding Last Day ad libitum (VAS-PF-AD, n = 5), VAS-Pair-feeding Last Day 4 meals (VAS-PF-4M, n = 5) (B) Body mass of ZL and ZF on VAD AD, VAS-PF AD and VAS-PF 4M. (C) Cumulative feed efficiency (unit weight gain per unit diet consumed) of ZL and ZF on VAD-AD, VAS-PF-AD and VAS-PF-4M. * Indicates p<0.05 using one-way ANOVA with LSD post-hoc test.
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pone-0100868-g004: The food intake, body mass and cumulative feed efficiency over 56 days of dietary manipulation.(A) Two-day food intake of ZL and ZF on VAD ad libitum (VAD-AD, n = 5), VAS-Pair-feeding Last Day ad libitum (VAS-PF-AD, n = 5), VAS-Pair-feeding Last Day 4 meals (VAS-PF-4M, n = 5) (B) Body mass of ZL and ZF on VAD AD, VAS-PF AD and VAS-PF 4M. (C) Cumulative feed efficiency (unit weight gain per unit diet consumed) of ZL and ZF on VAD-AD, VAS-PF-AD and VAS-PF-4M. * Indicates p<0.05 using one-way ANOVA with LSD post-hoc test.

Mentions: During the 56-day pair-feeding regimen, the two-day food intake of VAD-AD ZL rats gradually increased from ∼10 g initially to ∼40 g on days 33–34, and kept relatively stable until days 41–42 (Figure 4A, left panel). As anticipated [13]–[15], the food intake then started to decline until the end of the dietary manipulation. The two-day food intake of VAD-AD ZF rats quickly rose from ∼10 g initially to ∼60 g on days 17–18, leveled off between days 20 to 34, started to decline on days 35–36, reached ∼30 g on days 47–48, and leveled off again until the end of the dietary manipulation (right panel). During the same period, all VAS pair-fed ZL and ZF rats received the same amount of the isocaloric VAS diet to match the energy intake of VAD-AD rats. The body mass of VAD-AD ZL and ZF rats ceased to increase after 36 days of dietary manipulation (Figure 4B). From day 34, the body mass of VAD-AD ZL or ZF rats was significantly lower than that of VAS-PF ZL or ZF rats, respectively (marked by *). Furthermore, the cumulative feed efficiency of all three groups decreased over time. However, VAS-PF ZL or ZF rats had significantly higher feed efficiency than VAD-AD ZL or ZF rats after 36 or 22 days, respectively (Figure 4C).


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)

The food intake, body mass and cumulative feed efficiency over 56 days of dietary manipulation.(A) Two-day food intake of ZL and ZF on VAD ad libitum (VAD-AD, n = 5), VAS-Pair-feeding Last Day ad libitum (VAS-PF-AD, n = 5), VAS-Pair-feeding Last Day 4 meals (VAS-PF-4M, n = 5) (B) Body mass of ZL and ZF on VAD AD, VAS-PF AD and VAS-PF 4M. (C) Cumulative feed efficiency (unit weight gain per unit diet consumed) of ZL and ZF on VAD-AD, VAS-PF-AD and VAS-PF-4M. * Indicates p<0.05 using one-way ANOVA with LSD post-hoc test.
© Copyright Policy
Related In: Results  -  Collection

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

pone-0100868-g004: The food intake, body mass and cumulative feed efficiency over 56 days of dietary manipulation.(A) Two-day food intake of ZL and ZF on VAD ad libitum (VAD-AD, n = 5), VAS-Pair-feeding Last Day ad libitum (VAS-PF-AD, n = 5), VAS-Pair-feeding Last Day 4 meals (VAS-PF-4M, n = 5) (B) Body mass of ZL and ZF on VAD AD, VAS-PF AD and VAS-PF 4M. (C) Cumulative feed efficiency (unit weight gain per unit diet consumed) of ZL and ZF on VAD-AD, VAS-PF-AD and VAS-PF-4M. * Indicates p<0.05 using one-way ANOVA with LSD post-hoc test.
Mentions: During the 56-day pair-feeding regimen, the two-day food intake of VAD-AD ZL rats gradually increased from ∼10 g initially to ∼40 g on days 33–34, and kept relatively stable until days 41–42 (Figure 4A, left panel). As anticipated [13]–[15], the food intake then started to decline until the end of the dietary manipulation. The two-day food intake of VAD-AD ZF rats quickly rose from ∼10 g initially to ∼60 g on days 17–18, leveled off between days 20 to 34, started to decline on days 35–36, reached ∼30 g on days 47–48, and leveled off again until the end of the dietary manipulation (right panel). During the same period, all VAS pair-fed ZL and ZF rats received the same amount of the isocaloric VAS diet to match the energy intake of VAD-AD rats. The body mass of VAD-AD ZL and ZF rats ceased to increase after 36 days of dietary manipulation (Figure 4B). From day 34, the body mass of VAD-AD ZL or ZF rats was significantly lower than that of VAS-PF ZL or ZF rats, respectively (marked by *). Furthermore, the cumulative feed efficiency of all three groups decreased over time. However, VAS-PF ZL or ZF rats had significantly higher feed efficiency than VAD-AD ZL or ZF rats after 36 or 22 days, respectively (Figure 4C).

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