Importance Of HNF4-alpha In Liver Health (and Possibly Androgenic Alopecia)

Elephanto

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May 21, 2015
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Hepatic hepatocyte nuclear factor 4α is essential for maintaining triglyceride and cholesterol homeostasis
http://www.ncbi.nlm.nih.gov/pubmed/21071704
"reduced hepatic Hnf4α expression and resulted in striking phenotypes, including the development of fatty liver and a >80% decrease in plasma levels of triglycerides, total cholesterol, and high-density lipoprotein cholesterol.

Hepatocyte Nuclear Factor 4α Coordinates a Transcription Factor Network Regulating Hepatic Fatty Acid Metabolism
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2812226/
"Liver-specific inactivation of HNF4α leads to hepatomegaly and abnormal deposition of glycogen and lipid in the liver (13). Lipid accumulation in liver has been attributed to selective disruption of very-low-density lipoprotein (VLDL) secretion due to the downregulation of apolipoprotein B (ApoB) and microsomal triglyceride transfer protein (MTTP) expression "

http://www.ncbi.nlm.nih.gov/pubmed/11158324
"increased serum bile acid concentrations" (in lack of hnf4-alpha)

Factors influencing positively HNF4-alpha :

Preservation of hepatocyte nuclear factor-4α contributes to the beneficial effect of dietary medium chain triglyceride on alcohol-induced hepatic lipid dyshomeostasis in rats
http://www.ncbi.nlm.nih.gov/pubmed/23126616

Peroxisome proliferator-activated receptor activation by a short-term feeding of zingerone in aged rats
http://www.ncbi.nlm.nih.gov/pubmed/19459736
Collectively, our findings suggest that zingerone exerts its potent anti-inflammatory action by increasing HNF-4 and PPAR activities, while suppressing NF-kappaB activity.
(zingerone = component of ginger extract)

Zinc supplementation reverses alcohol-induced steatosis in mice through reactivating hepatocyte nuclear factor-4alpha and peroxisome proliferator-activated receptor-alpha
http://www.ncbi.nlm.nih.gov/pubmed/1963 ... $=activity

Factors influencing negatively HNF4-alpha :

Tumour suppressor p53 downregulates the expression of the human hepatocyte nuclear factor 4alpha (HNF4alpha) gene
http://www.ncbi.nlm.nih.gov/pubmed/16895524

Potential Role of Tumor Necrosis Factor-α in Downregulating Sex Hormone–Binding Globulin
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3266423/
"TNF-α–induced reduction of SHBG expression was mediated by downregulating HNF4A"

Monosaccharide-induced lipogenesis regulates the human hepatic sex hormone-binding globulin gene.
http://www.ncbi.nlm.nih.gov/pubmed/17992261
"monosaccharide-induced lipogenesis reduced hepatic HNF-4alpha levels, which in turn attenuated SHBG expression. inhibition of lipogenesis prevented monosaccharide-induced downregulation of HNF-4alpha and reduced SHBG expression"


This is what I've found so far. This could explain why some people (including myself) since Peating might have gotten a fatty liver from excess sugar (milk, honey, fruits) and I've personally had a report of elevated bilirubin fitting with the mention of elevated serum bile acids. The important part is to inhibit lipogenesis, but it seems counterproductive to me to eat a diet mostly made of sugar when the direct effect is induction of lipogenesis and downregulation of hnf4-a and it probably isn't suited for unoptimal livers or if for any reason your P53/TNF-alpha is elevated (iron overload from hemochromatosis for instance, which I might have). Carbs that are not sugar do not produce this effect. If you guys find other factors influencing hnf4-a, please share!

edit :

There's also a link with androgenic alopecia there.

Fatty liver <-> reduced hnf4-a <-> reduced shbg

In most studies, low shbg correlates with mpb.
 

ddjd

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This is what I've found so far. This could explain why some people (including myself) since Peating might have gotten a fatty liver from excess sugar (milk, honey, fruits) and I've personally had a report of elevated bilirubin fitting with the mention of elevated serum bile acids. The important part is to inhibit lipogenesis, but it seems counterproductive to me to eat a diet mostly made of sugar when the direct effect is induction of lipogenesis and downregulation of hnf4-a and it probably isn't suited for unoptimal livers or if for any reason your P53/TNF-alpha is elevated (iron overload from hemochromatosis for instance, which I might have). Carbs that are not sugar do not produce this effect. If you guys find other factors influencing hnf4-a, please share!
i also have high billirubin, so does it mean i have fatty liver?
 

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