scholarly journals Hepatic oxidation of choline and arsenocholine

1938 ◽  
Vol 32 (6) ◽  
pp. 1024-1032 ◽  
Author(s):  
Philip Jocelyn George Mann ◽  
Hubert Edmund Woodward ◽  
Juda Hirsch Quastel
Keyword(s):  
Hepatic Oxidation

scholarly journals Effects of propionate and carnitine on the hepatic oxidation of short- and medium-chain-length fatty acids

1988 ◽  
Vol 250 (3) ◽  
pp. 819-825 ◽  
Author(s):  
E P Brass ◽  
R A Beyerinck
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Organic Acid ◽  
Chain Length ◽  
Ketone Body ◽  
Acetyl Coa ◽  
Body Formation ◽  
Medium Chain ◽  
Medium Chain Length ◽  
Hepatic Oxidation

Accumulation of propionate, or its metabolic product propionyl-CoA, can disrupt normal cellular metabolism. The present study examined the effects of propionate, or propionyl-CoA generated during the oxidation of odd-chain-length fatty acids, on hepatic oxidation of short- and medium-chain-length fatty acids. In isolated hepatocytes, ketone-body formation from odd-chain-length fatty acids was slow as compared with even-chain-length fatty acid substrates, and increased as the carbon chain length was increased from five to seven to nine. In contrast, rates of ketogenesis from butyrate, hexonoate and octanoate were all approximately equal. Propionate (10 mM) inhibited ketogenesis from butyrate, hexanoate and octanoate by 81%, 53% and 18% respectively. Addition of carnitine had no effect on ketogenesis from the even-chain-length fatty acids, but increased the rate of ketone-body formation from pentanoate (by 53%), heptanoate (by 28%) and from butyrate or hexanoate in the presence of propionate. The inhibitory effect of propionate could not be explained by shunting acetyl-CoA into the tricarboxylic acid cycle, as CO2 formation from butyrate was also decreased by propionate. Examination of the hepatocyte CoA pool during oxidation of butyrate demonstrated that addition of propionate decreased acetyl-CoA and CoA as propionyl-CoA accumulated. Addition of carnitine decreased propionyl-CoA by 50% (associated with production of propionylcarnitine) and increased acetyl-CoA and CoA. Similar changes in the CoA pool were seen during the oxidation of pentanoate. These results demonstrate that accumulation of propionyl-CoA results in inhibition of short-chain fatty acid oxidation. Carnitine can partially reverse this inhibition. Changes in the hepatocyte CoA pool are consistent with carnitine acting by generating propionylcarnitine, thereby decreasing propionyl-CoA and increasing availability of free CoA. The data provide further evidence of the potential cellular toxicity from organic acid accretion, and supports the concept that carnitine's interaction with the cellular CoA pool can have a beneficial effect on cellular metabolism and function under conditions of unusual organic acid accumulation.

ENZYMATIC AND METABOLIC ADAPTATIONS: I. CHANGES IN INTACT RATS SUBJECTED TO DIETARY MODIFICATIONS

1962 ◽  
Vol 40 (1) ◽  
pp. 953-960 ◽  
Author(s):  
J. S. Willmer ◽  
T. S. Foster
Keyword(s):  
Liver Glycogen ◽  
Standard Laboratory ◽  
Hepatic Enzymes ◽  
Metabolic Adaptations ◽  
Hepatic Oxidation ◽  
Low Glucose ◽  
Oxidation Of Glucose ◽  
Dietary Modifications ◽  
Enzyme Changes ◽  
Intact Rats

A study of hepatic enzymes concerned in glucose metabolism was made after transfer of rats from a standard laboratory ration to three experimental diets. The change to two high-carbohydrate diets resulted in elevated levels of enzymes of the hexosemonophosphate shunt. Glucose-6-phosphatase, phosphoglucomu-tase, and phosphoglucoseisomerase exhibited an initial transitory decrease in activity, succeeded by restoration to normal or above-normal levels. Animals fed a low-glucose diet showed a tendency towards decreased activity of all enzymes except glucose-6-phosphatase. Hepatic oxidation of glucose-1-C14and glucose-6-C14and liver glycogen levels were also measured. These results are discussed in relation to the observed enzyme changes.

Drives and limits to feed intake in ruminants

2014 ◽  
Vol 54 (10) ◽  
pp. 1513 ◽  
Author(s):  
Michael S. Allen
Keyword(s):  
Feed Intake ◽  
Feeding Behaviour ◽  
General Circulation ◽  
Physiological State ◽  
Vagal Afferents ◽  
Energy Status ◽  
Hepatic Oxidation ◽  
Ruminant Diets ◽  
Lactation Cycle ◽  
Osmotic Effects

The control of energy intake is complex, including mechanisms that act independently (e.g. distention, osmotic effects, fuel-sensing) as well as interacting factors that are likely to affect feeding via their effects on hepatic oxidation. Effects of ruminant diets on feed intake vary greatly because of variation in their filling effects, as well as the type and temporal absorption of fuels. Effects of nutrients on endocrine response and gene expression affect energy partitioning, which in turn affects feeding behaviour by altering clearance of fuels from the blood. Dominant mechanisms controlling feed intake change with physiological state, which is highly variable among ruminants, especially through the lactation cycle. Ruminal distention might dominate control of feed intake when ruminants consume low-energy diets or when energy requirements are high, but fuel-sensing by tissues is likely to dominate control of feed intake when fuel supply is in excess of that required. The liver is likely to be a primary sensor of energy status because it is supplied by fuels from the portal drained viscera as well as the general circulation, it metabolises a variety of fuels derived from both the diet and tissues, and a signal related to hepatic oxidation of fuels is conveyed to feeding centres in the brain by hepatic vagal afferents stimulating or inhibiting feeding, depending on its energy status. The effects of somatotropin on export of fuels by milk secretion, effects of insulin on gluconeogenesis, and both on mobilisation and repletion of tissues, determine fuel availability and feed intake over the lactation cycle. Control of feed intake by hepatic energy status, affected by oxidation of fuels, is an appealing conceptual model because it integrates effects of various fuels and physiological states on feeding behaviour.

Kinetic parameters of hepatic oxidation of cyclic fatty acid monomers formed from linoleic and linolenic acids

2001 ◽  
Vol 12 (10) ◽  
pp. 554-558 ◽  
Author(s):  
Florent Joffre ◽  
Jean-Charles Martin ◽  
Martine Genty ◽  
Luc Demaison ◽  
Olivier Loreau ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Kinetic Parameters ◽  
Cyclic Fatty Acid ◽  
Cyclic Fatty Acid Monomers ◽  
Hepatic Oxidation

Plasma oxyphytosterol concentrations originate from hepatic oxidation and subsequent spill-over in the circulation

2020 ◽  
Vol 315 ◽  
pp. e160-e161
Author(s):  
S. Baumgartner ◽  
D. Lütjohann ◽  
B. Groen ◽  
R.P. Mensink ◽  
J. Plat
Keyword(s):  
Hepatic Oxidation

Hormonal regulation of hepatic glycine oxidation

1993 ◽  
Vol 44 (3) ◽  
pp. 473 ◽  
Author(s):  
M Jois ◽  
JT Brosnan
Keyword(s):  
Direct Effect ◽  
Hormonal Regulation ◽  
Inorganic Phosphate ◽  
Protein S ◽  
Calcium Mobilization ◽  
The Other ◽  
Isolated Mitochondria ◽  
Cytosolic Protein ◽  
Hepatic Oxidation ◽  
Stimulation Of

Hormones which regulate hepatic oxidation of glycine include glucagon, catecholamines and vasopressin. The stimulation of oxidation of glycine by glucagon requires cyclic nucleotidedependent phosphorylation of one or more cytosolic proteins and does not involve mobilization of calcium from intracellular stores. The stimulation of glycine oxidation by catecholamines and vasopressin, on the other hand, appears to involve calcium mobilization. While calcium has direct effect on mitochondrial glycine oxidation, the link between phosphorylation of cytosolic protein(s) and mitochondrial glycine oxidation is not known. The stimulation of glycine oxidation by hormones can be demonstrated in mitochondria isolated from rats treated with hormones prior to sacrifice. Both the effects of glucagon and calcium are evident in isolated mitochondria only when inorganic phosphate is included in the medium. These findings are discussed in relation to the regulation of hepatic glycine oxidation.

scholarly journals Hepatic oxidation of the stereoisomers of methionine hydroxyanalogue in chicks

1990 ◽  
Vol 30 (1) ◽  
pp. 137-137
Author(s):  
L. Dupuis ◽  
P. Brachet ◽  
A. Puigserver
Keyword(s):  
Hepatic Oxidation

Control of eating by hepatic oxidation of fatty acids. A note of caution

Appetite ◽  
2009 ◽  
Vol 53 (2) ◽  
pp. 272-273 ◽  
Author(s):  
Michael S. Allen ◽  
Barry J. Bradford
Keyword(s):  
Fatty Acids ◽  
Hepatic Oxidation
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