New study sheds more light on
gene-diet interactions in obese adults. Genes are one of the many factors
that can cause obesity and type 2 diabetes which are the variables of metabolic
The ADIPOQ gene with many of its variants is one such contributor to these
disorders. This gene instructs the production of h
adiponectin in the fat cells. Adiponectin is a protein hormone that plays a
role in the insulin sensitivity, glucose metabolism and fat burning.
increases insulin sensitivity by burning fatty acids and inhibiting the
production of glucose in the liver.
Studies have found that some ADIPOQ
gene variants are responsible for
lower adiponectin concentrations in the blood. Decreased adiponectin
concentration means less efficient fat burning and less glucose utilization and
therefore a greater risk of developing type-2 diabetes and obesity. However,
this happens only in those people who carry this 'risk variant' of ADIPOQ
There are ways to increase blood
adiponectin levels. Interestingly, studies have found evidence of gene - diet
interactions in obesity
. They claim that people who are risk variant carriers
can improve their adiponectin through certain nutrients, especially fatty
So, Aseel AlSaleh and colleagues
at Kings College London, School of Medicine, London, conducted a trial to find
out how dietary n3 PUFAs such as fish oil interacts with adiponectin gene (ADIPOQ
variant to affect blood adinopectin concentration.
This study included 142 healthy
men and 225 women aged 45-70 years for 12 months from which only 310 people
completed the study.
The researchers randomly assigned
daily doses of 0.45, 0.9, and 1.8 g 20:5n3 and 22:6n3 (1.51:1), or placebo, in
3 capsules taken as dietary supplements. Oily fish intake was restricted to 1
portion per month throughout the 12-month period.
Blood samples for the analysis of
plasma lipids, glucose, and insulin and serum adiponectin were drawn after a
minimum 8-hour overnight fast preceded by a low-fat evening meal.
DNA testing of five ADIPOQ
gene variants [−11391 G/A
(rs17300539), −11377 C/G (rs266729), −10066 G/A (rs182052), +45 T/G
(rs2241766), and +276 G/T (rs1501299)] was done.
The researchers found that serum
adiponectin concentration significantly increased in subjects more than 58
, and that too after the highest dose (1.8 g/d) of fish oil
'If aging is associated with
development of adiponectin resistance, the increase observed in only the oldest
participants may reflect an ability to respond only after a high intake of n3
PUFA,' they analyzed.
They also found that the interaction among SNP
+45 T/G genotype, treatment, and age was only nominally significant as far as
serum adiponectin is concerned. Earlier studies have shown that +45 TT genotype
(risk gene variant) is associated with lower serum adiponectin and increased
risk of type 2 diabetes, obesity, and adverse metabolic marker. The researchers
thus reasoned 'interaction of the +45 TT
genotype with high-dose n3 PUFA supplements may serve a protective function in
susceptible older individuals
They concluded that older people who have +45 TT genotype may reduce
the risk of metabolic syndrome associated type 2 diabetes and obesity if they
increase the consumption of fish oil.
'A recommendation to +45 TT
homozygotes to increase consumption of oily fish to maintain adiponectin
concentrations with advancing years would be justified,' they reported.
The study is published in Journal of Nutrition.