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Anti Sweet Carving Hormone Discovered by Scientists

A Liver hormone which switches off the preference for sugary foods has been found by scientists; The research could improve diet and help patients who are diabetic or obese.

dessert-sweet,   food illustration 352475_640


We all love our sugar, especially during the holidays. Cookies, cake, and candy are simply irresistible.

While sugar cravings are common, the physiological mechanisms that trigger our “sweet tooth” are not well defined.

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A University of Iowa-led study in mice shows that a hormone produced by the liver, fibroblast growth factor 21 (FGF21), suppresses the consumption of simple sugars. The researchers report that FGF21 is produced in the liver in response to high carbohydrate levels. FGF21 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.

The research could improve diet and help patients who are diabetic or obese.

“We’ve known for a while that FGF21 can enhance insulin sensitivity, ” says Lucas BonDurant, a Co-first author, “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.”

“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?”



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