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. 
 
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 Paper 1: Cell Metabolism, von Holstein-Rathlou and BonDurant et al: "FGF21 Mediates Endocrine Control of Simple Sugar Intake and Sweet Taste Preference by the Liver" http://dx. doi. org/ 10. 1016/ j. cmet. 2015. 12. 003 
 
 The study was funded in part by grants from the American Diabetes Association, the National Institutes of Health, the Edward Mallinckrodt Jr. Foundation, the University of Iowa Fraternal Order of Eagles Diabetes Research Center, and the Novo Nordisk Foundation Center for Basic Metabolic Research. 
 
 Paper 2: Cell Metabolism, Talukdar and Owen et al: "FGF21 Regulates Sweet and Alcohol Preference" http://dx. doi. org/ 10. 1016/ j. cmet. 2015. 12. 008 
 
 This work was supported by the National Institutes of Health, the Robert A. Welch Foundation, the Sir Henry Dale Fellowship jointly funded by the Wellcome Trust and the Royal Society, the Ford Foundation Fellowship, the German National Science Foundation, and the Howard Hughes Medical Institute. 

 A cure for sugar cravings is a major step nearer after scientists identified a hormone which suppresses a "sweet tooth". 
 
 Researchers say their findings, published online in the journal Cell Metabolism, could improve the diet and help patients who are diabetic or obese. 
 
 While sugar cravings are common, particularly at this time of year, the physiological mechanisms that trigger our " sweet tooth " were not well defined until now. 
 
 "FGF21 can help people who might not be able to sense when they've had enough sugar, which may contribute to diabetes" 
 
 But the new study in mice shows that a hormone produced by the liver, fibroblast growth factor 21 (FGF21), suppresses the consumption of simple sugars. 
 
 The researchers say that FGF21 is produced in the liver in response to high carbohydrate levels. The hormone then enters the bloodstream, where it sends a signal to the brain to suppress the preference for sweets. 
 
 The study's co-senior author Doctor Matthew Potthoff, assistant professor of pharmacology in the University of Iowa in the US, said: "This is the first liver-derived hormone we know that regulates sugar intake specifically." 
 
 Previous research explains how certain hormones affect appetite; however, these hormones don't regulate any specific macronutrient - carbohydrate, protein, fat - and are produced by organs other than the liver. 
 
 Co-first author Lucas BonDurant, a doctoral student, said: "We've known for a while that FGF21 can enhance insulin sensitivity. 
 
 "Now, there's this dimension where FGF21 can help people who might not be able to sense when they've had enough sugar, which may contribute to diabetes." 
 
 The work is based on human genome-wide studies where researchers found associations between certain DNA mutations and people's intake of specific macronutrients. 
 
 Two of the mutations were located near the FGF21 gene, prompting the researchers to identify the role of this hormone in regulating macronutrient preference. 
 
 They used genetically-engineered mouse models and pharmacological approaches to examine the role of FGF21 in regulating sugar cravings. 
 
 In normal mice, they injected FGF21 and gave the mice a choice between a normal diet and a sugar-enriched diet. They observed that the mice didn't completely stop eating sugar, but they ate seven times less than normal. 
 
 The researchers also studied genetically-modified mice that either didn't produce FGF21 at all or produced a lot of FGF21 - over 500 times more than normal mice. 
 
 The genetically-modified mice had a choice between the same two diets as the normal mice. 
 
 The researchers observed that the mice that didn't produce FGF21 at all ate more sugar, whereas the mice that produced a lot of FGF21 ate less sugar. 
 
 Based on the results, they concluded that FGF21 decreases appetite and intake of sugar. 
 
 However, FGF21 does not reduce intake of all sugars - sucrose, fructose, and glucose - equally. FGF21 also doesn't impact the intake of complex carbohydrates. 
 
 While the researchers found that FGF21 sends signals to the brain, they say additional work is necessary to identify the precise neural pathways that regulate FGF21's ability to manage macronutrient preference. 
 
 The research team are focused on the hypothalamus - a section of the brain responsible for regulating eating behaviour and energy homeostasis. 
 
 Dr Potthoff added: "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. 
 
 "If so, how do those signals intertwine to regulate the neural sensing of different macronutrients?" 

 Still desperate for another candy bar or cocktail, but don’t know why? Never fear - US scientists have found a liver hormone that could curb our sugar and alcohol cravings, and help those suffering from diabetes or obesity. 
 
 Two independent research groups have found a hormone produced by the liver (fibroblast growth factor 21, or FGF21) that suppresses the desire to consume simple sugars, the studies published in Cell Metabolism suggest. 
 
 The hormone is produced if the level of carbohydrates is high, in which case it enters the bloodstream and sends a signal to the brain to curb the craving. 
 
 The findings are unprecedented, researchers say. Earlier, only appetite-controlling hormones were known. 
 
 "This is the first liver-derived hormone we know that regulates sugar intake specifically," said Matthew Potthoff, assistant professor of pharmacology at the University of Iowa, and co-senior author of one of the papers. 
 
 READ MORE: Chemical that makes you ‘feel full’ could be weight-loss wonder drug 
 
 "We never imagined that a circulating, liver-derived factor would exist whose function is to control sweet appetite,” his co-senior author Matthew Gillum, of the University of Copenhagen, added. "We are very excited about investigating this hormonal pathway further." 
 
 One reason FGF21 exists in animals could be to improve diet quality, the scientists said. Another possibility, since sugar can ferment, was that it helped the liver protect itself from excess alcohol. 
 
 "FGF21 can exert powerful effects on behavior by acting on the central nervous system, including in humans," Steven Kliewer of University of Texas Southwestern Medical Center, and senior author of the other study, said. 
 
 How can the discovery be used? 
 
 First and foremost, the findings can help people with diabetes, as well as those “who might not be able to sense when they've had enough sugar, which may contribute to diabetes,” according to co-first author Lucas BonDurant. 
 
 In one of the studies, researchers used genetically-engineered mice, injecting FGF21 and giving the mice a choice between a normal diet and a sugar-enriched diet. As a result, the mice didn’t stop eating sugary foods altogether, but ate seven times less. 
 
 In a different experiment, scientists studied genetically-modified mice that either didn't produce FGF21 at all, or produced over 500 times more of the hormone than normal mice. The former ate more sugar, while the latter consumed less, researchers found. 
 
 READ MORE: Diabetes, obesity linked to chemical exposure – Endocrine Society 
 
 The same hormone suppresses the consumption of sweets in primates, another study discovered. A single dose could cause a monkey to almost immediately lose interest in sweet water, researchers said, adding that they were struck by the powerful effect of FGF21. 
 
 All in all, the study concluded that FGF21 decreases appetite and intake of sugar. 
 
 Now scientists want to find out the exact neural pathways that regulate FGF21's ability to manage macronutrient preference. 
 
 "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 said. 
 
 READ MORE: Secret of binging: Stress drives desire ‘for reward, not pleasure’ 
 
 Kliewer, however, has cautioned against pronouncing the findings 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," he said. 

 (A and B) Hepatic Fgf21 mRNA (A) and plasma FGF21 protein (B) levels in 11- to 13-week-old male WT C57Bl/6 mice ad libitum fed chow and provided water, 0.2% saccharin (sacc), 10% glucose (gluc), 10% fructose (fruc), or 10% sucrose (sucr) ad libitum in a drinking bottle for 24 hr (n = 5/group). 
 
 (C and D) Hepatic Fgf21 mRNA (C) and plasma FGF21 protein (D) levels in 11- to 13-week-old male WT C57Bl/6 mice ad libitum fed chow and provided 10% sucrose ad libitum for the indicated time (n = 5/group). 
 
 (E and F) Hepatic Fgf21 mRNA (E) and plasma FGF21 protein (F) levels in 10- to 12-week-old male WT (FGF21fl/fl) and FGF21 liver-specific knockout (FGF21 LivKO) mice ad libitum fed chow and 10% sucrose ad libitum for 24 hr (n = 5–7/group). 
 
 (G) HSD preference ratio in 10- to 12-week-old male WT and FGF21 LivKO mice (n = 5/group). 
 
 (H) Plasma FGF21 levels in human subjects maintained at hyperglycemia via dextrose infusion for 0, 2, and 24 hr (n = 10). 
 
 (I) Plasma FGF21 levels in WT and ChREBP KO mice ad libitum fed chow and 10% sucrose ad libitum for 24 hr (n = 5–8/group). Values are represented as mean ± SEM (∗p < 0.05; ∗∗p < 0.01; ∗∗∗p < 0.005; ∗∗∗, #p < 0.001 compared to WT).
– The days of uncontrollably binging on leftover Christmas goodies may be numbered. The Telegraph reports researchers have figured out a hormone produced in the liver that reduces the desire to eat sugar. Fibroblast growth factor 21—or FGF21—is produced when carbohydrate levels in the body get too high and tells the brain to suppress the body's desire for sugar. "We never imagined that a circulating, liver-derived factor would exist whose function is to control sweet appetite,” RT quotes study co-author Matthew Gillum as saying. Hormones have been known to suppress appetites as a whole but never individual types of nutrients. "This is the first liver-derived hormone we know that regulates sugar intake specifically," says researcher Dr. Matthew Potthoff of the University of Iowa. According to the study—published in Cell Metabolism—mice born with an FGF21 deficiency ate more sugar, while those born with an excess of the hormone ate much less. But it doesn't have to be left up to nature. Researchers found mice injected with FGF21 ate seven times less sugar, the Telegraph reports. A second study found a similar effect in primates given a dose of the hormone, according to a press release. This could be good news for obese people or those with diabetes. "FGF21 can help people who might not be able to sense when they've had enough sugar," researcher Lucas BonDurant says. According to the press release, the same hormone could also suppress the desire for alcohol. (Speaking of sugar, there's a senator in charge of stocking a candy desk.)