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  #1   ^
Old Wed, Apr-18-18, 03:51
teaser's Avatar
teaser teaser is offline
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Default Surprising discovery: Sweet tooth gene connected with less body fat

https://www.sciencedaily.com/releas...80411111013.htm

Quote:
People with a gene variation of FGF21 have a predisposition to less body fat than others, new research conducted at the University of Copenhagen, among others, shows.

It comes as a bit of a surprise to the researchers, who last year discovered that precisely this genetic variation could be one of the reasons why some people have a particular craving for sweet things. People with this variation eat more sugar than others.

'It sort of contradicts common intuition that people who eat more sugar should have less body fat. But it is important to remember that we are only studying this specific genetic variation and trying to find connections to the rest of the body. This is just a small piece of the puzzle describing the connection between diet and sugar intake and the risk of obesity and diabetes', says one of the researchers behind the study, Associate Professor Niels Grarup from the Novo Nordisk Foundation Center for Basic Metabolic Research.

Higher Blood Pressure and More 'Apple Shape'

But the effects associated with the genetic variation are not all positive, the new study shows. The genetic variation is connected with slightly increased blood pressure and more fat around the waist than the hips -- that is, more 'apple shape'.

The study is an international collaboration headed by researchers at the University of Exeter Medical School and has just been published in the scientific journal Cell Reports.

The researchers' conclusions are based on large amounts of data. They have studied health information from more than 450,000 individuals who have allowed their data to be recorded in the UK Biobank. It includes blood samples, questionnaires on diet and genetic data, among other things.

'Now that so many people are involved in the study, it gives our conclusions a certain robustness. Even though the difference in the amount of body fat or blood pressure level is only minor depending on whether or not the person has this genetic variation or not, we are very confident that the results are accurate. Around 20 per cent of the European population has this genetic predisposition', says Niels Grarup.

Potential Drug Target

This new knowledge about people with a 'genetic sweet tooth' is mainly important in connection with the development of drugs and future research. Because researchers are currently trying to determine whether it is possible to target or replace FGF21 using drugs in order to treat for obesity and diabetes.

'Due to its connection with sugar, FGF21 constitutes a potential target in the treatment of for example obesity and diabetes. This research helps us to understand the underlying mechanisms of the hormone and to predict its effects and side effects', says Niels Grarup.

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  #2   ^
Old Wed, Apr-18-18, 04:20
teaser's Avatar
teaser teaser is offline
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I don't really find this that surprising. In animal studies, fructose's claim to fame isn't that it's especially fattening, it's that it induces insulin resistance and type II diabetes. We flinch when a diet that makes rats fat is described as "high fat" when it is also high in sugar--but high sugar in and of itself doesn't make the animals nearly as fat, generally, though it will give them symptoms of metabolic syndrome.

An interesting aspect of this, you see the model of excess fat in adipose, and then spillover to visceral/liver etc. fat then causing insulin resistance, but the liver is involved in various ways with regulation of body fat, there is the possibility that signalling from the liver, or just more constantly elevated insulin levels, makes the adipose tissue less insulin sensitive, so that overall fatness decreases even though insulin is higher.

Stephen Guyunet has a post here;

http://wholehealthsource.blogspot.c...er-nail-in.html

that might relate, he uses it that argue that insulin isn't fattening.

Quote:
In the first study, published in 1980 by Dr. Dennis A. Vanderweele and colleagues, rats were implanted with mini-pumps delivering insulin at a steady rate throughout the day and night for 7 days (4). They tested four different doses: 0, 1, 2 and 6 units per day, and measured food intake and body weight. This is a model of chronically elevated insulin reminiscent of what is seen in insulin-resistant people.

They found that all doses of insulin reduced body weight gain, but only the 2 unit dose was statistically significant. They speculated that the 6 unit dose was less effective at reducing weight gain because it was sufficiently high to cause hypoglycemia (low blood sugar), which is a potent trigger for food intake. Total food intake was suppressed at all doses by insulin as well, but this was apparently not due to illness. The authors conclude:
1) insulin limits meal size when blood levels are modestly elevated for prolonged periods of time in the rat, 2) this decrease in meal size is not compensated for by an increase in meal frequency and, hence, total daily food ingestion and body weight gain are reduced, and 3) this effect appears to be a heightening of satiety rather than an induction of illness.


Notice the bit about hypoglycemia. If this model induces insulin resistance--I would expect an animal with otherwise normal function would upregulate various counterregulatory hormones pretty much continuously, or downregulate insulin receptors etc., or some combination--a lack of a fattening effect might not be surprising. In contrast, there's a mouse model where inducing hypoglycemia through insulin once a week does induce substantial weight gain.

What happens when an animal eats? Initially, before there's much in the way of nutrient absorption, there's a small initial burst of insulin that serves to reduce nutrients in the blood. You might get this walking by a bakery, suddenly feel hungry. That small burst might be absent if you're insulin resistant--absent or insufficient first phase insulin response figures big in the Newcastle studies. Even a normal insulin response should send a weaker signal if the basal insulin levels are elevated.

Type II patients still getting fatter when they use exogenous insulin makes perfect sense--they're able to add enough to blast past the resistance, perhaps it's more the large boluses for meals that's fattening rather than the basal insulin.
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  #3   ^
Old Wed, Apr-18-18, 07:16
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GRB5111 GRB5111 is offline
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The original study with the genetic variant causing a predisposition to less body fat even with more sugar consumption makes sense. It's what many refer to as TOFI. The real question is how healthy are these individuals after consuming so much sugar despite no outward (visible) symptoms.
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  #4   ^
Old Wed, Apr-18-18, 09:26
teaser's Avatar
teaser teaser is offline
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The spin they gave this story is horrendous.

Quote:
But the effects associated with the genetic variation are not all positive,


Not all positive--arguably, none of the effects are positive, if maximum safer subcutaneous fat is maxed out sooner and spillover into liver etc. happens sooner. Picture of a happy thin lady about to gorge on cake to boot.
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  #5   ^
Old Wed, Apr-18-18, 19:39
M Levac M Levac is offline
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Quote:
'Due to its connection with sugar, FGF21 constitutes a potential target in the treatment of for example obesity and diabetes. This research helps us to understand the underlying mechanisms of the hormone and to predict its effects and side effects', says Niels Grarup.

This didn't make sense to me because the whole article seems to be about a gene. So I went looking and found that FGF21 is Fibroblast growth factor 21, a hormone. I don't normally rely on Wiki for info, still I found this (https://en.wikipedia.org/wiki/FGF21):
Quote:
In liver FGF21 expression is regulated by PPARα and levels rise substantially with both fasting and consumption of ketogenic diets.

If we accept the premise that FGF21 is associated with a sweet tooth, we can easily accept that a ketogenic diet would trigger that sweet tooth by the same mechanisms that activate FGF21, i.e. PPAR-a and so forth. Then there's this:
Quote:
FGF21 stimulates glucose uptake in adipocytes but not in other cell types.

If this is true, and if eating sugar activates FGF21, it supports the typical Taubes hypothesis - carbs drive insulin drive excess fat accumulation, and glucose into fat cells -> glycerol -> triglycerides can't get out. Also if this is true, the association found with lower body fat must be incorrect.

On the other hand, if a ketogenic diet activates FGF21, and if FGF21 stimulates glucose uptake in adipocytes but not in other cells, it explains tight regulation of fat release from fat cells during ketosis (rather than loose regulation that woud allow a runaway effect), and partly explains BG drop as well.

I won't delve into the resources used for that Wiki page, I'm not that interested in FGF21. I get the impression it's a pointy target with a marginal potential. Also it sounds like the drug they're developing based on that research is a free pass to eat all the sugar we want, rather than a genuine medical treatment.
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  #6   ^
Old Thu, Apr-19-18, 03:57
teaser's Avatar
teaser teaser is offline
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Plan: mostly milkfat
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Quote:
People with a gene variation of FGF21


I'll have to look deeper into this, but I don't think the researchers are claiming that FGF21 does damage. The hormone is increased in fatty liver, but it's thought to be a protective response, and FGF21 is being looked at as a possible therapeutic agent. We're looking at a variation of FGF21, these people's hormone may just not work as well as other people's, or they may secrete less or something. It's not FGF21 that's associated with the sweet tooth, it's the particular variant.
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  #7   ^
Old Fri, Apr-20-18, 07:27
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WereBear WereBear is offline
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Quote:
Originally Posted by GRB5111
The real question is how healthy are these individuals after consuming so much sugar despite no outward (visible) symptoms.


Quote:
Originally Posted by teaser
Not all positive--arguably, none of the effects are positive, if maximum safer subcutaneous fat is maxed out sooner and spillover into liver etc. happens sooner. Picture of a happy thin lady about to gorge on cake to boot.


You guys said what I was going to say

This turning-sugar-into-fat is considered an adaptation to store fat in fall to draw upon during the lean months of winter. Bears and chipmunks do it; we just don't hibernate.

As such, I consider it a gene that would be more active closer to the poles of the Earth than the equator, and in my random noticing, I see that.

I went to my brother's wedding in Rio de Janeiro, and these are petite folks (I look like Attack of the 50 Foot Woman in the wedding photos) who can dance all night on a diet that is 80% starch.
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