Half the country has the diabetes gene?????



http://www.ajcn.org/cgi/content/abstract/85/1/102

FABP2 Ala54Thr genotype is associated with glucoregulatory function
and lipid oxidation after a high-fat meal in sedentary nondiabetic men
and women1,2,3
Edward P Weiss, Josef Brandauer, Onanong Kulaputana, Ioana A Ghiu,
Christopher R Wohn, Dana A Phares, Alan R Shuldiner and James M
Hagberg
1 From the Department of Kinesiology, University of Maryland, College
Park, MD (EPW, JB, OK, IAG, CRW, DAP, and JMH); the Division of
Endocrinology, Diabetes, and Nutrition, University of Maryland School
of Medicine, Baltimore, MD (ARS); and the Geriatric Research Education
and Clinical Center, Baltimore Veterans Administration Medical Center,
Baltimore, MD (ARS)


Background: A common functional missense mutation [Ala54Thr of the
fatty acid-binding protein 2 gene (FABP2)] has previously been studied
for associations with glucoregulation, postprandial lipemia, and lipid
oxidation rates. However, most of those studies have not accounted for
the interactive and potentially confounding effects of habitual
physical activity and diet.

Objective: We tested the hypothesis that, in sedentary nondiabetic
subjects following a low-fat diet, Thr54 FABP2 carriers have lower
glucoregulatory function, greater postprandial lipemia, and greater
lipid oxidation rates than do their Ala54 FABP2-homozygous
counterparts.

Design: Men and women (n = 122) aged 50-75 y who were following a low-
fat diet were genotyped and underwent oral-glucose-tolerance tests. A
subgroup (n = 36) also underwent postprandial lipemia tests with lipid
oxidation rate measurements.

Results: Thr54 carriers were less likely to have normal glucose
tolerance (P = 0.05) and had higher fasting glucose concentrations (P
= 0.003) than did Ala54 homozygotes. In Thr54 carriers, the insulin
sensitivity index was lower (P = 0.02), and the fasting insulin and
the oral-glucose-tolerance test insulin area under the curve were
higher (P = 0.05 and 0.03, respectively) than in Ala54 homozygotes.
FABP2 genotype was not associated with fasting or postprandial lipemia
test triacylglycerol or free fatty acids (P 0.22 for all), but
postprandial lipid oxidation rates were higher (P = 0.01), which
suggests that fat absorption is higher in Thr54 carriers than in Ala54
homozygotes.

Conclusions: In sedentary nondiabetic persons following a low-fat
diet, FABP2 Thr54 carriers have lower glucose tolerance and lower
insulin action than do Ala54-homozygous persons. Furthermore, FABP
Thr54 carriers have higher lipid oxidation rates, which may be the
mechanism of glucoregulatory dysfunction.

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Quite the extrapolation. Test 122 people and apply those findings to
the entire 298,444,215 population. Amazing how the press has blindly
accepted that "Half the country has the diabetes gene" from a sampling
of 122.

Whatever happened to the insistence by food industry cultists of the
need for "properly set up trials" and far reaching massive
epidemiological studies and large scale multi-million dollar double
blind studies etc, to prove any minor scientific point being studied.

Talk about double standards in scientific proof.

TC

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