J. Girard

Publications195
h-index59
Citations13,193
Highly Influential Citations601
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Contribution of de novo fatty acid synthesis to hepatic steatosis and insulin resistance: lessons from genetically engineered mice.
TLDR
A review of recent advances in the field of nonalcoholic fatty liver disease discusses recent advances and suggests that modulating important enzymes in fatty acid synthesis in liver may be key for the treatment of NAFLD.
Transient increase in obese gene expression after food intake or insulin administration
TLDR
It is shown that ob gene exhibits diurnal variation, increasing during the night, after rats start eating, which is linked to changes in food intake, as fasting prevented the cyclic variation and decreased ob messenger RNA.
Hepatic Glucokinase Is Required for the Synergistic Action of ChREBP and SREBP-1c on Glycolytic and Lipogenic Gene Expression*
TLDR
It is demonstrated that in hGK-KO hepatocytes overexpressing SREBP-1c, the effect of glucose on glycolytic and lipogenic genes is lost because of the impaired ability of these hepatocytes to efficiently metabolize glucose, despite a marked increase in low Km hexokinase activity.
Polyunsaturated fatty acids suppress glycolytic and lipogenic genes through the inhibition of ChREBP nuclear protein translocation.
TLDR
A novel mechanism to explain the inhibitory effect of PUFAs on the genes encoding L-PK and FAS is described and it is demonstrated that ChREBP is a pivotal transcription factor responsible for coordinating the PUFA suppression of glycolytic and lipogenic genes.
ChREBP, a transcriptional regulator of glucose and lipid metabolism.
TLDR
Some of the studies that have begun to elucidate the regulation and function of this key transcription factor in liver are reviewed.
Liver-Specific Inhibition of ChREBP Improves Hepatic Steatosis and Insulin Resistance in ob/ob Mice
TLDR
It is demonstrated that ChREBP is central for the regulation of lipogenesis in vivo and plays a determinant role in the development of the hepatic steatosis and of insulin resistance in ob/ob mice.
Carbohydrate responsive element binding protein (ChREBP) and sterol regulatory element binding protein-1c (SREBP-1c): two key regulators of glucose metabolism and lipid synthesis in liver.
The lipogenic transcription factor ChREBP dissociates hepatic steatosis from insulin resistance in mice and humans.
TLDR
It is demonstrated that increased ChREBP can dissociate hepatic steatosis from insulin resistance, with beneficial effects on both glucose and lipid metabolism.
ChREBP, but not LXRs, is required for the induction of glucose-regulated genes in mouse liver.
TLDR
It is demonstrated that glucose is required for ChREBP functional activity and that LXRs are not necessary for the induction of glucose-regulated genes in liver.
Control of gene expression by fatty acids.
TLDR
The last decade provided evidence that major or minor dietary constituents regulated gene expression in an hormonal-independent manner, but molecular mechanisms by which fatty acids control the expression genes encoding regulatory protein involved in their own metabolism are reviewed.
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