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Linoleic acid responsible for human obesity in 20th century
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Taka
Nov 4, 2012, 3:24:08 AM11/4/12
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Dietary Linoleic Acid Elevates Endogenous
2-AG and Anandamide and Induces Obesity
Suppressing hyperactive endocannabinoid tone is a critical target for
reducing obesity. The backbone of both
endocannabinoids 2-arachidonoylglycerol (2-AG) and anandamide (AEA) is
the ω-6 fatty acid arachidonic acid (AA).
Here we posited that excessive dietary intake of linoleic acid (LA),
the precursor of AA, would induce endocannabinoid
hyperactivity and promote obesity. LA was isolated as an independent
variable to reflect the dietary increase in
LA from 1 percent of energy (en%) to 8 en% occurring in the United
States during the 20th century. Mice were fed
diets containing 1 en% LA, 8 en% LA, and 8 en% LA + 1 en%
eicosapentaenoic acid (EPA) + docosahexaenoic acid
(DHA) in medium-fat diets (35 en% fat) and high-fat diets (60 en%) for
14 weeks from weaning. Increasing LA from
1 en% to 8 en% elevated AA-phospholipids (PL) in liver and
erythrocytes, tripled 2-AG + 1-AG and AEA associated
with increased food intake, feed efficiency, and adiposity in mice.
Reducing AA-PL by adding 1 en% long-chain ω-3
fats to 8 en% LA diets resulted in metabolic patterns resembling 1 en%
LA diets. Selectively reducing LA to 1 en%
reversed the obesogenic properties of a 60 en% fat diet. These animal
diets modeled 20th century increases of human
LA consumption, changes that closely correlate with increasing
prevalence rates of obesity. In summary, dietary LA
increased tissue AA, and subsequently elevated 2-AG + 1-AG and AEA
resulting in the development of diet-induced
obesity. The adipogenic effect of LA can be prevented by consuming
sufficient EPA and DHA to reduce the AA-PL
pool and normalize endocannabinoid tone.
Obesity (2012) 20, 1984–1994. doi:10.1038/oby.2012.38
PDF: http://www.nature.com/oby/journal/v20/n10/pdf/oby201238a.pdf
2-AG and Anandamide and Induces Obesity
Suppressing hyperactive endocannabinoid tone is a critical target for
reducing obesity. The backbone of both
endocannabinoids 2-arachidonoylglycerol (2-AG) and anandamide (AEA) is
the ω-6 fatty acid arachidonic acid (AA).
Here we posited that excessive dietary intake of linoleic acid (LA),
the precursor of AA, would induce endocannabinoid
hyperactivity and promote obesity. LA was isolated as an independent
variable to reflect the dietary increase in
LA from 1 percent of energy (en%) to 8 en% occurring in the United
States during the 20th century. Mice were fed
diets containing 1 en% LA, 8 en% LA, and 8 en% LA + 1 en%
eicosapentaenoic acid (EPA) + docosahexaenoic acid
(DHA) in medium-fat diets (35 en% fat) and high-fat diets (60 en%) for
14 weeks from weaning. Increasing LA from
1 en% to 8 en% elevated AA-phospholipids (PL) in liver and
erythrocytes, tripled 2-AG + 1-AG and AEA associated
with increased food intake, feed efficiency, and adiposity in mice.
Reducing AA-PL by adding 1 en% long-chain ω-3
fats to 8 en% LA diets resulted in metabolic patterns resembling 1 en%
LA diets. Selectively reducing LA to 1 en%
reversed the obesogenic properties of a 60 en% fat diet. These animal
diets modeled 20th century increases of human
LA consumption, changes that closely correlate with increasing
prevalence rates of obesity. In summary, dietary LA
increased tissue AA, and subsequently elevated 2-AG + 1-AG and AEA
resulting in the development of diet-induced
obesity. The adipogenic effect of LA can be prevented by consuming
sufficient EPA and DHA to reduce the AA-PL
pool and normalize endocannabinoid tone.
Obesity (2012) 20, 1984–1994. doi:10.1038/oby.2012.38
PDF: http://www.nature.com/oby/journal/v20/n10/pdf/oby201238a.pdf
John H. Gohde
Nov 4, 2012, 8:46:20 AM11/4/12
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epidemic.
http://tinyurl.com/9xapzgr
Just thought that you might want to know.
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