Portal hypothesis

The portal-visceral hypothesis describes a possible mechanism for some of the health effects of obesity, particularly the metabolic syndrome. It says that obesity (especially visceral obesity) results in increased circulation of free fatty acids and thus, via Randle's effect, in insulin resistance.[1]

The word "portal" refers to the hepatic portal circulation from the digestive system to the liver. The portal-visceral hypothesis is a replacement for the earlier "portal hypothesis", which said that visceral obesity leads to an increase in fatty acid levels specifically in the portal vein.

References

Heilbronn, L.; Smith, S. R.; Ravussin, E. (1 January 2004). "Failure of fat cell proliferation, mitochondrial function and fat oxidation results in ectopic fat storage, insulin resistance and type II diabetes mellitus". Int J Obes Relat Metab Disord. 28 (S4): S12–S21. doi:10.1038/sj.ijo.0802853. PMID 15592481.

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[1] Heilbronn, L.; Smith, S. R.; Ravussin, E. (1 January 2004). "Failure of fat cell proliferation, mitochondrial function and fat oxidation results in ectopic fat storage, insulin resistance and type II diabetes mellitus". Int J Obes Relat Metab Disord. 28 (S4): S12–S21. doi:10.1038/sj.ijo.0802853. PMID 15592481.