当前位置： SCI文献检索 > GENOME BIOLOGY期刊下所有文献 > Hepatic steatosis risk is partly driven by increased de novo lipogenesis following carbohydrate consumption.

Hepatic steatosis risk is partly driven by increased de novo lipogenesis following carbohydrate consumption.

Abstract：

BACKGROUND:Diet is a major contributor to metabolic disease risk, but there is controversy as to whether increased incidences of diseases such as non-alcoholic fatty liver disease arise from consumption of saturated fats or free sugars. Here, we investigate whether a sub-set of triacylglycerols (TAGs) were associated with hepatic steatosis and whether they arise from de novo lipogenesis (DNL) from the consumption of carbohydrates. RESULTS:We conduct direct infusion mass spectrometry of lipids in plasma to study the association between specific TAGs and hepatic steatosis assessed by ultrasound and fatty liver index in volunteers from the UK-based Fenland Study and evaluate clustering of TAGs in the National Survey of Health and Development UK cohort. We find that TAGs containing saturated and monounsaturated fatty acids with 16-18 carbons are specifically associated with hepatic steatosis. These TAGs are additionally associated with higher consumption of carbohydrate and saturated fat, hepatic steatosis, and variations in the gene for protein phosphatase 1, regulatory subunit 3b (PPP1R3B), which in part regulates glycogen synthesis. DNL is measured in hyperphagic ob/ob mice, mice on a western diet (high in fat and free sugar) and in healthy humans using stable isotope techniques following high carbohydrate meals, demonstrating the rate of DNL correlates with increased synthesis of this cluster of TAGs. Furthermore, these TAGs are increased in plasma from patients with biopsy-confirmed steatosis. CONCLUSION:A subset of TAGs is associated with hepatic steatosis, even when correcting for common confounding factors. We suggest that hepatic steatosis risk in western populations is in part driven by increased DNL following carbohydrate rich meals in addition to the consumption of saturated fat.

journal_name

Genome Biol

journal_title

Genome biology

authors

Sanders FWB,Acharjee A,Walker C,Marney L,Roberts LD,Imamura F,Jenkins B,Case J,Ray S,Virtue S,Vidal-Puig A,Kuh D,Hardy R,Allison M,Forouhi N,Murray AJ,Wareham N,Vacca M,Koulman A,Griffin JL

doi

10.1186/s13059-018-1439-8

subject

Has Abstract

pub_date

2018-06-20 00:00:00

pages

issue

eissn

1474-7596

issn

1474-760X

pii

10.1186/s13059-018-1439-8

journal_volume

pub_type

杂志文章

在线工具

Hepatic steatosis risk is partly driven by increased de novo lipogenesis following carbohydrate consumption.