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  #1   ^
Old Wed, Mar-08-17, 15:11
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Default Regulation of simple sugar intake by the liver

https://www.sciencedaily.com/releas...51225141547.htm

Quote:
Liver may sway sweet tooth, alcohol consumption

It may be your liver (and not your better judgement) that keeps you away from excess sweets this holiday season. Two independent research groups have found the first evidence of a liver-derived hormone that specifically regulates intake of sugars and alcohol in mice. One of the studies also found that the same hormone suppresses the consumption of sweets in primates.

"A lot of work has examined the central mechanisms regulating sugar-seeking behavior, but the post-ingestive mechanisms regulating sugar appetite are poorly understood," says Matthew Potthoff of the University of Iowa, a senior author on one of the papers.

"We never imagined that a circulating, liver-derived factor would exist whose function is to control sweet appetite, says his co-senior author Matthew Gillum of the University of Copenhagen. "We are very excited about investigating this hormonal pathway further."

The studies, together with human genetics studies linking the hormone--called FGF21 (or fibroblast growth factor 21)--to nutrient preference, "show that FGF21 can exert powerful effects on behavior by acting on the central nervous system, including in humans," says Steven A. Kliewer of University of Texas Southwestern Medical Center, a senior author on the other paper.

He adds one note of caution: "While at first blush it would seem that this FGF21-regulated pathway could be a panacea for suppressing sugar and alcohol consumption, it's important to keep in mind that these reward behaviors are closely tied to mood, and so additional studies to determine if FGF21 causes depression are certainly warranted."

The study from the lab of Kliewer and David J. Mangelsdorf at UT Southwestern and collaborators at Pfizer looked at FGF21 in both mice and monkeys. He says that while many signaling pathways in the central nervous systems are known to influence sweet and alcohol preference, this is the first liver-derived hormone found to have these effects. He was also struck by how powerfully FGF21 could suppress appetite, as a single dose could cause a monkey to almost immediately lose interest in sweet water.

But how is FGF21 working? In the other study, led by Potthoff and Gillum, they showed that, in mice, the liver produces FGF21 in response to sugar intake. FGF21 then enters the bloodstream and selectively suppresses sugar appetite by acting on the hypothalamus, a part of the brain that regulates food intake and energy homeostasis.

"In addition to identifying these neural pathways, we would like to see if additional hormones exist to regulate appetite for specific macronutrients like fat and protein, comparable to the effects of FGF21 on carbohydrate intake," Potthoff says. "If so, how do those signals intertwine to regulate the neural sensing of different macronutrients?"

Studies from over 50 years ago suggested that the liver was an important regulator of food intake and preference. Previous work has also shown that FGF21 is derived primarily from the liver, and that variations in the FGF21 gene sequence are associated with changes in macronutrient preference in humans. All of this together led Potthoff and Gillum to evaluate the role of FGF21 in regulating food preference.

We can only speculate why FGF21 exists in animals: Does it improve diet quality, preventing junk food consumption? Or, since sugar can ferment into ethanol, does it help the liver protect itself from excess alcohol? Whatever its origin, its ability to prevent overconsumption of sugar could be harnessed therapeutically upon further investigation in humans and could help explain why analogs of FGF21 are currently undergoing clinical evaluation for the treatment of obesity and type 2 diabetes.

Both groups agree that more work is needed, but the studies add to the growing evidence that--from gut microbes to our organs--controlling appetite is a whole-body affair.


I guess not too too surprising, the liver is forced to do most of the work of metabolizing fructose and alcohol, why shouldn't it have a role in suppressing further intake? Lol at "suppressing junk food consumption." Even an animal whose entire diet is made up of fruit needs to know when it's had enough fructose.
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Old Thu, Mar-09-17, 05:58
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As non-alcoholic fatty liver disease develops, does the liver lose this ability?
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Old Thu, Mar-09-17, 08:10
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https://www.ncbi.nlm.nih.gov/pubmed/25736301

Quote:
Role of fibroblast growth factor 21 in the early stage of NASH induced by methionine- and choline-deficient diet.

Tanaka N1, Takahashi S2, Zhang Y3, Krausz KW2, Smith PB4, Patterson AD4, Gonzalez FJ5.
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Abstract
Fibroblast growth factor 21 (FGF21) is a modulator of energy homeostasis and is increased in human nonalcoholic liver disease (NAFLD) and after feeding of methionine- and choline-deficient diet (MCD), a conventional inducer of murine nonalcoholic steatohepatitis (NASH). However, the significance of FGF21 induction in the occurrence of MCD-induced NASH remains undetermined. C57BL/6J Fgf21-null and wild-type mice were treated with MCD for 1 week. Hepatic Fgf21 mRNA was increased early after commencing MCD treatment independent of peroxisome proliferator-activated receptor (PPAR) α and farnesoid X receptor. While no significant differences in white adipose lipolysis were seen in both genotypes, hepatic triglyceride (TG) contents were increased in Fgf21-null mice, likely due to the up-regulation of genes encoding CD36 and phosphatidic acid phosphatase 2a/2c, involved in fatty acid (FA) uptake and diacylglycerol synthesis, respectively, and suppression of increased mRNAs encoding carnitine palmitoyl-CoA transferase 1α, PPARγ coactivator 1α, and adipose TG lipase, which are associated with lipid clearance in the liver. The MCD-treated Fgf21-null mice showed increased hepatic endoplasmic reticulum (ER) stress. Exposure of primary hepatocytes to palmitic acid elevated the mRNA levels encoding DNA damage-inducible transcript 3, an indicator of ER stress, and FGF21 in a PPARα-independent manner, suggesting that lipid-induced ER stress can enhance hepatic FGF21 expression. Collectively, FGF21 is elevated in the early stage of MCD-induced NASH likely to minimize hepatic lipid accumulation and ensuing ER stress. These results provide a possible mechanism on how FGF21 is increased in NAFLD/NASH.


It seems to ge a general defense vs. fatty liver. So it's elevated in fatty liver. I don't know if this is a matter of "FGF21 resistance" or just a matter of the modern diet being sort of above its paygrade. I'm sure it means well.

Methionine and choline deficient diets--methionine and choline-rich diets both stand accused in some vegan circles of being deathogenic, methionine restriction studies in mice show increased longevity. And byproducts of choline metabolism by some gut bugs yields a substance (TMAO) that's accused of causing heart disease. A fair number of people are probably avoiding choline and methionine in their diet, I'm sure that will end well.
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