Studies on the ethanol-induced decrease of fatty acid oxidation in rat and human liver slices

Coconut oil (CO) induces a triacylglycerol infiltration in the hepatocytes of preruminant calves when given as the sole source of fat in the milk diet over a long-term period. Metabolic pathways potentially involved in this hepatic triacylglycerol accumulation were studied by in vitro methods on liver slices from preruminant Holstein × Friesian male calves fed a conventional milk diet containing CO (n 5) or beef tallow (BT, n 5) for 19 d. Liver slices were incubated for 12 h in the presence of 0·8 mM-[14C] oleate or -[14C] laurate added to the medium. Fatty acid oxidation was determined by measuring the production of CO2 (total oxidation) and acid-soluble products (partial oxidation). Production of CO2 was 1·7–3·6-fold lower (P 0·0490) and production of acid-soluble products tended to be lower (P = 0·0625) in liver slices of CO- than BT-fed calves. Fatty acid esterification as neutral lipids was 2·6– to 3·1–fold higher (P = 0·0088) in liver slices prepared from calves fed the CO diet compared with calves fed the BT diet. By contrast with what occurs in the liver of rats fed CO, the increase in neutral lipid production did not stimulate VLDL secretion by the hepatocytes of calves fed with CO, leading to a triacylglycerol accumulation in the cytosol. It could be explained by the reduction of fatty acid oxidation favouring esterification in the form of triacylglycerols, in association with a limited availability of triacylglycerols and/or apolipoprotein B for VLDL packaging and subsequent secretion.

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Studies on the control of fatty acid oxidation in liver preparations from chick embryos

Canadian Journal of Biochemistry ◽

10.1139/o70-068 ◽

1970 ◽

Vol 48 (4) ◽

pp. 418-424 ◽

Cited By ~ 11

Author(s):

D. J. Koerker ◽

I. B. Fritz

Keyword(s):

Fatty Acid ◽

Fatty Acid Oxidation ◽

Respiratory Control ◽

Liver Mitochondria ◽

Acid Oxidation ◽

Chick Embryos ◽

Stage Of Development ◽

Liver Slices ◽

Hepatic Fatty Acid Oxidation ◽

Carnitine Palmitoyltransferase Activity

The characteristics and developmental pattern of the metabolic pathway for fatty acid oxidation were investigated in liver slices and mitochondria prepared from chick embryos of varying ages. In 8-day-old chick embryos, hepatic fatty acid oxidation was readily measurable. The incorporation of labelled palmitate into CO2 was increased twofold by carnitine in liver slices of 8-day-old chick embryos but by nearly sixfold to tenfold in tissues prepared from 10- or 12-day-old embryos. A similar increase was seen in the degree of augmentation of ketogenesis induced by carnitine in liver slices prepared from the 10-day-old embryo, suggesting an increased carnitine palmitoyltransferase activity in liver cells during the stage of development from 8 to 10 days. Palmitoyl-CoA was not metabolized in the absence of carnitine, whereas the palmitoyl portion of palmitoylcarnitine readily supported respiration by embryonic chick liver mitochondria. In the presence of adequate amounts of albumin, good respiratory control was evident.The administration of glucose to chick eggs which had previously been incubated for approximately 4.5 days resulted in changes in the metabolism of embryos killed 5 days later, which indicated that tissues of the chick embryo were capable of integrative metabolic adaptations in response to changes in substrate supply.

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Adiponectin Upregulates SHBG Production: Molecular Mechanisms and Potential Implications

Endocrinology ◽

10.1210/en.2014-1072 ◽

2014 ◽

Vol 155 (8) ◽

pp. 2820-2830 ◽

Cited By ~ 34

Author(s):

Rafael Simó ◽

Cristina Saez-Lopez ◽

Albert Lecube ◽

Cristina Hernandez ◽

Jose Manuel Fort ◽

...

Keyword(s):

Fatty Acid ◽

Fatty Acid Oxidation ◽

Lipid Content ◽

Hepg2 Cells ◽

Human Liver ◽

Acid Oxidation ◽

Hepatic Lipid ◽

Human Liver Biopsies ◽

Liver Biopsies ◽

Hepatic Lipid Content

Epidemiological studies have shown that plasma SHBG levels correlate with plasma adiponectin levels, both in men and women. There are no reports describing any molecular mechanism by which adiponectin regulates hepatic SHBG production. The aim of the present study is to explore whether adiponectin regulates SHBG production by increasing HNF-4α levels through reducing hepatic lipid content. For this purpose, in vitro studies using human HepG2 cells, as well as human liver biopsies, were performed. Our results show that adiponectin treatment increased SHBG production via AMPK activation in HepG2 cells. Adiponectin treatment decreased the mRNA and protein levels of enzymes related to hepatic lipogenesis (ACC) and increased those related to fatty acid oxidation (ACOX and CPTI). These adiponectin-induced changes in hepatic enzymes resulted in a reduction of total TG and FFA and an increase of HNF-4α. When HNF-4α expression was silenced by using siRNA, adiponectin-induced SHBG overexpression was blocked. Furthermore, adiponectin-induced upregulation of SHBG production via HNF-4α overexpression was abrogated by the inhibition of fatty acid oxidation or by the induction of lipogenesis with a 30mM glucose treatment in HepG2 cells. Finally, adiponectin levels correlated positively and significantly with both HNF-4α and SHBG mRNA levels in human liver biopsies. Our results suggest for the first time that adiponectin increases SHBG production by activating AMPK, which reduces hepatic lipid content and increases HNF-4α levels.

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