Systematic studies have shown that providing individuals
with larger portions of foods and beverages leads to substantial increases in
energy intake. The effect is sustained over weeks, supporting the possibility
that large portions have a role in the development of obesity. The challenge is
to find strategies to effectively manage the effects of portion size. One
approach involves teaching people to select appropriate portions and to use
tools that facilitate portion control….A more effective strategy may be to
encourage people to increase the proportion of foods low in energy density in
their diets while limiting portions of high-energy-dense foods. If people lower
the energy density of their diet, they can eat satisfying portions while
managing their body weight.
In reality this is common knowledge. I am reminded of the
day I brought one of my Czech partners and his family out to lunch in Boston. The
portions arrived and they were aghast. The plate was about 18” across in an
oval and it was piled high with food. I explained that they were not expected
to finish the meal. Then I turned around and saw the Americans devouring the
plates and then ordering deserts, all of them obese or morbidly obese. In
Prague our lunch was on a small plate and like almost all Czechs they had a 6
oz glass of beer. Portion size is both cultural and personal. Just because it
is placed in front of you there is no need to eat all of it. Thus in my opinion
the Rolls paper is typical of many, an attempt to shift the blame.
Rolls concludes:
In an obesogenic environment where large portions of
energy-dense foods are pervasive and viewed as appropriate, it is challenging
to find effective strategies to help people consume portions that match their
energy requirements. Although there are a number of tools to teach people to
recognize appropriate portions, it is not clear that these tools produce
sustained changes in eating behavior that facilitate weight management.
There is a simple
tool, the scale. Weigh yourself. The problem is that we all too often shift the
blame to some third party. The solution lies within themselves, self-control.
Now to the second article by Suh et al. As VoA remarks[1]:
Scientists have known about the protein, called FGF1, for
several decades. But researchers discovered the potential of the molecule,
which is part of a family of so-called growth factors, when they injected it
into mice that were engineered to have Type 2 - or adult-onset - diabetes. The
blood sugar levels of the experimental animals were restored to a healthy range
for more than two days after a single injection.
Now Suh and the authors state:
Fibroblast growth factor 1 (FGF1) is an
autocrine/paracrine regulator whose binding to heparan sulphate proteoglycans
effectively precludes its circulation. Although FGF1 is known as a mitogenic
factor, FGF1 knockout mice develop insulin resistance when stressed by a
high-fat diet, suggesting a potential role in nutrient homeostasis. Here we
show that parenteral delivery of a single dose of recombinant FGF1 (rFGF1)
results in potent, insulin-dependent lowering of glucose levels in diabetic
mice that is dose-dependent but does not lead to hypoglycaemia. Chronic
pharmacological treatment with rFGF1 increases insulin-dependent glucose uptake
in skeletal muscle and suppresses the hepatic production of glucose to achieve
whole-body insulin sensitization. The sustained glucose lowering and insulin
sensitization attributed to rFGF1 are not accompanied by the side effects of
weight gain, liver steatosis and bone loss associated with current
insulin-sensitizing therapies. We also show that the glucose-lowering activity
of FGF1 can be dissociated from its mitogenic activity and is mediated
predominantly via FGF receptor 1 signalling. Thus we have uncovered an
unexpected, neomorphic insulin-sensitizing action for exogenous non-mitogenic
human FGF1 with therapeutic potential for the treatment of insulin resistance
and type 2 diabetes.
The problem is that many of the insulin stimulating drugs
for Type 2 Diabetes do not solve the underlying problem of chronic
inflammation. That seems only solvable by a restricted dies and weight loss.
Thus FGF1 is an interesting approach it still may not solve the underlying set
of issues found in obesity. The problem is first obesity and then its sequella,
increased blood sugar.
References:
Rolls, B., What is the role of portion control in weight
management? International Journal of Obesity (2014) 38, S1–S8. http://www.nature.com/ijo/journal/v38/n1s/full/ijo201482a.html
Suh, J., et al, Endocrinization of FGF1 produces a
neomorphic and potent insulin sensitizer, Nature, July 2014. http://www.nature.com/nature/journal/vaop/ncurrent/full/nature13540.html
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