Relation of hepatic ketogenesis to radiation-induced decrease in fasting ketonemia

1960 ◽  
Vol 198 (1) ◽  
pp. 33-36
Author(s):  
Joseph A. Ontko
Keyword(s):  
Fatty Acid ◽  
Oxidase Activity ◽  
Ketone Bodies ◽  
Liver Mitochondria ◽  
Whole Body ◽  
Acid Oxidation ◽  
Hepatic Glycogen ◽  
Acid Oxidase ◽  
Liver Slices ◽  
Radiation Induced

Male, weanling rats were exposed to 500 r of whole-body x-irradiation and then fasted. Control rats were concurrently fasted. Ketonemia, ketonuria, hepatic glycogen, ketogenesis by liver slices and fatty acid oxidase activity of liver mitochondria were measured. A radiation-induced decrease in fasting ketonemia was observed. This decrease was mainly in the ß-hydroxybutyric acid fraction. Ketonuria was similar in both control and irradiated lots the 1st postirradiation day and lower in the irradiated lot during the 2nd day. Decreased ketonemia in the irradiated rats, which exhibited diuresis, was thus apparently not due to increased urinary excretion of ketone bodies. Ketogenesis by liver slices from irradiated rats was depressed. This indicated that an antiketogenic process contributed to the radiation-induced decrease in fasting ketonemia. Fatty acid oxidase activity of liver mitochondria isolated from control and irradiated rats was similar. Thus, rate-limiting fatty acid oxidizing enzymes were not altered by radiation under these conditions. This illustrates an apparent modifying effect of other cellular fractions on fatty acid oxidation in mitochondria.

scholarly journals Development of fatty acid oxidation in neonatal guinea-pig liver

1982 ◽  
Vol 208 (3) ◽  
pp. 723-730 ◽  
Author(s):  
D A Shipp ◽  
M Parameswaran ◽  
I J Arinze
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Guinea Pig ◽  
Ketone Bodies ◽  
Liver Mitochondria ◽  
Fatty Acyl ◽  
Acid Oxidation ◽  
Beta Oxidation ◽  
Pig Liver ◽  
Guinea Pig Liver

The capacity of foetal and neonatal liver to oxidize short-, medium- and long-chain fatty acids was studied in the guinea pig. Liver mitochondria from foetal and newborn animals were unable to synthesize ketone bodies from octanoate, but octanoylcarnitine and palmitoylcarnitine were readily ketogenic. The ketogenic capacity at 24 h after birth was as high as in adult animals. Hepatocytes isolated from term animals were unable to oxidize fatty acids, but at 6 h after birth production of 14CO2, acid-soluble products and acetoacetate from 1-14C-labelled fatty acids was 40-50% of the rates at 24 h. At 12 h of age these rates had already reached the 24 h values and did not change during suckling in the first week of life. The activities of hepatic fatty acyl-CoA synthetases, which were minimal in the foetus or at term, increased to maximal values in 12-24 h. The data show that the capacity for beta-oxidation and ketogenesis develops maximally in this species during the first 6-12 h after birth, and appears to be partly dependent on the development of fatty acid-activating enzyme.

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

1970 ◽  
Vol 48 (4) ◽  
pp. 418-424 ◽  
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.

Whole body energy expenditure and fuel oxidation after 2,5-anhydro-D-mannitol administration

1995 ◽  
Vol 268 (1) ◽  
pp. R299-R302 ◽  
Author(s):  
C. R. Park ◽  
R. J. Seeley ◽  
L. Benthem ◽  
M. I. Friedman ◽  
S. C. Woods
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Food Intake ◽  
Ketone Bodies ◽  
Whole Body ◽  
Acid Oxidation ◽  
Metabolic Variables ◽  
Continued Use ◽  
Body Energy ◽  
Lines Of Evidence

The fructose analogue 2,5-anhydro-D-mannitol (2,5-AM) increases food intake in nondeprived rats. Several lines of evidence indicate that vagal signals arising from the liver are critical for this effect. In addition, 2,5-AM decreases plasma glucose and increases lipolysis, resulting in an increase in plasma free fatty acids and ketone bodies. In these respects 2,5-AM produces a state analogous to that observed after food deprivation. Using an indirect calorimeter, we determined that 2,5-AM (300 mg/kg ip) causes a potent and long-lasting decrease in respiratory quotient, indicating a decrease in the fraction of total energy derived from carbohydrate oxidation and an increase in the fraction derived from fatty acid oxidation. These metabolic variables were altered without affecting total metabolic rate. This dose of analogue also stimulated significantly greater food intake than injections of vehicle. These results support the continued use of 2,5-AM as a tool to probe the metabolic controls of food intake.

scholarly journals Deletion of nuclear factor-κB p50 upregulates fatty acid utilization and contributes to an anti-obesity and high-endurance phenotype in mice

2015 ◽  
Vol 309 (6) ◽  
pp. E523-E533 ◽  
Author(s):  
Yoshihiko Minegishi ◽  
Satoshi Haramizu ◽  
Koichi Misawa ◽  
Akira Shimotoyodome ◽  
Tadashi Hase ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Nuclear Factor Κb ◽  
Whole Body ◽  
Acid Oxidation ◽  
Endurance Capacity ◽  
Peroxisome Proliferator ◽  
Primary Role ◽  
Nuclear Factor ◽  
Oxidation Activity ◽  
Fatty Acid Utilization

The transcription factor nuclear factor-κB (NF-κB) plays an important role in regulating physiological processes such as immunity and inflammation. In addition to this primary role, NF-κB interacts physically with peroxisome proliferator-activated receptors regulating lipid metabolism-related gene expression and inhibits their transcriptional activity. Therefore, inhibition of NF-κB may promote fatty acid utilization, which could ameliorate obesity and improve endurance capacity. To test this hypothesis, we attempted to elucidate the energy metabolic status of mice lacking the p50 subunit of NF-κB (p50 KO mice) from the tissue to whole body level. p50 KO mice showed a significantly lower respiratory quotient throughout the day than did wild-type (WT) mice; this decrease was associated with increased fatty acid oxidation activity in liver and gastrocnemius muscle of p50 KO mice. p50 KO mice that were fed a high-fat diet were also resistant to fat accumulation and adipose tissue inflammation. Furthermore, p50 KO mice showed a significantly longer maximum running time compared with WT mice, with a lower respiratory exchange ratio during exercise as well as higher residual muscle glycogen content and lower blood lactate levels after exercise. These results suggest that p50 deletion facilitates fatty acid catabolism, leading to an anti-obesity and high-endurance phenotype of mice and supporting the idea that NF-κB is an important regulator of energy metabolism.

Meal composition affects postprandial fatty acid oxidation

1993 ◽  
Vol 264 (6) ◽  
pp. R1065-R1070 ◽  
Author(s):  
D. M. Surina ◽  
W. Langhans ◽  
R. Pauli ◽  
C. Wenk
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Nutrient Utilization ◽  
Whole Body ◽  
Acid Oxidation ◽  
Plasma Ffa ◽  
Hepatic Fatty Acid Oxidation ◽  
Beta Hydroxybutyrate ◽  
Chain Fatty Acids

The influence of macronutrient content of a meal on postprandial fatty acid oxidation was investigated in 13 Caucasian males after consumption of a high-fat (HF) breakfast (33% carbohydrate, 52% fat, 15% protein) and after an equicaloric high-carbohydrate (HC) breakfast (78% carbohydrate, 6% fat, 15% protein). The HF breakfast contained short- and medium-chain fatty acids, as well as long-chain fatty acids. Respiratory quotient (RQ) and plasma beta-hydroxybutyrate (BHB) were measured during the 3 h after the meal as indicators of whole body substrate oxidation and hepatic fatty acid oxidation, respectively. Plasma levels of free fatty acids (FFA), triglycerides, glucose, insulin, and lactate were also determined because of their relationship to nutrient utilization. RQ was significantly lower and plasma BHB was higher after the HF breakfast than after the HC breakfast, implying that more fat is burned in general and specifically in the liver after an HF meal. As expected, plasma FFA and triglycerides were higher after the HF meal, and insulin and lactate were higher after the HC meal. In sum, oxidation of ingested fat occurred in response to a single HF meal.

Carnitine effects on palmitate-1-C14 conversion to CO2 and glycerides by various tissues

1964 ◽  
Vol 206 (6) ◽  
pp. 1217-1222 ◽  
Author(s):  
Irving B. Fritz
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Rat Heart ◽  
Liver Microsomes ◽  
Tissue Homogenate ◽  
Acid Oxidation ◽  
Acid Oxidase ◽  
Palmitate Oxidation ◽  
Glyceride Synthesis ◽  
Low Concentrations

Carnitine increased oxidation of palmitate-1-C14 by rat heart and liver preparations, but decreased palmitate incorporation into glycerides. To determine which of the effects was derivative and which was primary, experiments were repeated using tissues whose rates of fatty acid oxidation had been depressed by Amytal poisoning. Under these conditions, carnitine inhibition of fatty acid conversion to glycerides was abolished. Similarly, low concentrations of carnitine were found to enhance palmitate oxidation without influencing palmitate esterification. Isolated liver microsomes which synthesized glycerides without oxidizing fatty acids showed no response to carnitine under all conditions tried. The inability of carnitine to alter glyceride formation in experiments described may signify that acyl-CoA generation from CoA and acylcarnitine is specifically directed toward the fatty acid oxidase system rather than to glyceride synthesis. It was also shown that, under conditions optimal for demonstration of carnitine augmentation of fatty acid oxidation by rat heart preparations, carnitine increased palmitate oxidation by a variety of other tissue homogenate preparations.

Effect of adipocyte β3-adrenergic receptor activation on the type 2 diabetic MKR mice

2006 ◽  
Vol 290 (6) ◽  
pp. E1227-E1236 ◽  
Author(s):  
Hyunsook Kim ◽  
Patricia A. Pennisi ◽  
Oksana Gavrilova ◽  
Stephanie Pack ◽  
William Jou ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Receptor Activation ◽  
Whole Body ◽  
Acid Oxidation ◽  
Adrenergic Agonists ◽  
Nonobese Diabetic ◽  
Type 2 Diabetic

The antiobesity and antidiabetic effects of the β3-adrenergic agonists were investigated on nonobese type 2 diabetic MKR mice after injection with a β3-adrenergic agonist, CL-316243. An intact response to acute CL-316243 treatment was observed in MKR mice. Chronic intraperitoneal CL-316243 treatment of MKR mice reduced blood glucose and serum insulin levels. Hyperinsulinemic euglycemic clamps exhibited improvement of the whole body insulin sensitivity and glucose homeostasis concurrently with enhanced insulin action in liver and adipose tissue. Treating MKR mice with CL-316243 significantly lowered serum and hepatic lipid levels, in part due to increased whole body triglyceride clearance and fatty acid oxidation in adipocytes. A significant reduction in total body fat content and epididymal fat weight was observed along with enhanced metabolic rate in both wild-type and MKR mice after treatment. These data demonstrate that β3-adrenergic activation improves the diabetic state of nonobese diabetic MKR mice by potentiation of free fatty acid oxidation by adipose tissue, suggesting a potential therapeutic role for β3-adrenergic agonists in nonobese diabetic subjects.

scholarly journals AMPK as a mediator of hormonal signalling

2009 ◽  
Vol 44 (2) ◽  
pp. 87-97 ◽  
Author(s):  
Chung Thong Lim ◽  
Blerina Kola ◽  
Márta Korbonits
Keyword(s):  
Protein Synthesis ◽  
Fatty Acid ◽  
Metabolic Disorders ◽  
Energy Homeostasis ◽  
Metabolic Effects ◽  
Whole Body ◽  
Acid Oxidation ◽  
Treatment Of Obesity ◽  
Amp Activated Protein Kinase ◽  
Hormonal Signalling

AMP-activated protein kinase (AMPK) is a key molecular player in energy homeostasis at both cellular and whole-body levels. AMPK has been shown to mediate the metabolic effects of hormones such as leptin, ghrelin, adiponectin, glucocorticoids and insulin as well as cannabinoids. Generally, activated AMPK stimulates catabolic pathways (glycolysis, fatty acid oxidation and mitochondrial biogenesis) and inhibits anabolic pathways (gluconeogenesis, glycogen, fatty acid and protein synthesis), and has a direct appetite-regulating effect in the hypothalamus. Drugs that activate AMPK, namely metformin and thiazolidinediones, are often used to treat metabolic disorders. Thus, AMPK is now recognised as a potential target for the treatment of obesity and associated co-morbidities.

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