Hepatic vagotomy effects on metabolic challenges during parenteral nutrition in rats

1994 ◽  
Vol 266 (2) ◽  
pp. R646-R649 ◽  
Author(s):  
J. L. Beverly ◽  
Z. J. Yang ◽  
M. M. Meguid
Keyword(s):  
Fatty Acid ◽  
Parenteral Nutrition ◽  
Fatty Acid Oxidation ◽  
Latin Square ◽  
Plasma Free Fatty Acid ◽  
Acid Oxidation ◽  
Feeding Response ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Hepatic Fatty Acid Oxidation

During parenteral nutrition (PN) glucoprivic-induced feeding appeared to be neutralized by the oxidation of infused fatty acids. With the use of a latin-square design, the feeding response to 2-deoxy-D-glucose (2-DG) and/or 2-mercaptoacetate (MA) was evaluated in male Sprague-Dawley rats with hepatic branch vagotomy (HV) or sham operations (SO). Rats received continuous infusions of 0.9% saline or PN providing 100% of daily caloric needs (PN-100) for four consecutive days. During PN-100, food intake was stimulated by 2-DG in HV rats and when fatty acid oxidation was simultaneously inhibited by MA. 2-DG-induced hyperglycemia was apparent under all conditions. Lipoprivic-induced feeding and increased plasma free fatty acid concentrations were absent in HV rats, whether MA was administered alone or with 2-DG. The feeding response to glucoprivic challenges is influenced by the relative availability of alternate energy sources. The lack of feeding response to 2-DG during PN-100 is mediated by vagal input of hepatic fatty acid oxidation status.

Effect of adrenodemedullation on decline in muscle malonyl-CoA during exercise

1993 ◽  
Vol 74 (5) ◽  
pp. 2548-2551 ◽  
Author(s):  
W. W. Winder ◽  
R. W. Braiden ◽  
D. C. Cartmill ◽  
C. A. Hutber ◽  
J. P. Jones
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Treadmill Running ◽  
Acid Oxidation ◽  
Sham Operation ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Malonyl Coa ◽  
Exercise Induced ◽  
Rate Limiting

Malonyl-CoA is an inhibitor of carnitine palmitoyltransferase, a rate-limiting enzyme of fatty acid oxidation. Previous studies have indicated that muscle malonyl-CoA declines in rats during treadmill running. This decrease may be important for allowing an increased rate of fatty acid oxidation during prolonged exercise. This study was designed to determine whether epinephrine is essential for inducing the decline in muscle malonyl-CoA during exercise. Male Sprague-Dawley rats underwent adrenodemedullation (ADM) or sham operation. After allowing 3 wk for recovery, rats were killed (pentobarbital anesthesia) at rest or after running at 21 m/min up a 15% grade for 60 min. Red quadriceps malonyl-CoA decreased from 2.6 +/- 0.3 to 0.8 +/- 0.07 nmol/g in sham-operated rats and from 2.2 +/- 0.3 to 0.8 +/- 0.1 nmol/g in ADM rats. White quadriceps malonyl-CoA decreased to similar levels during exercise in both sham-operated and ADM rats. A second experiment on 24-h fasted rats also showed no impairment in the exercise-induced decline in red quadriceps malonyl-CoA as a result of adrenodemedullation. The hormones of the adrenal medulla are therefore unessential for inducing the decline in malonyl-CoA during exercise.

2-Mercaptoacetate, an inhibitor of fatty acid oxidation, decreases the membrane potential in rat liver in vivo

1999 ◽  
Vol 277 (1) ◽  
pp. R301-R305 ◽  
Author(s):  
Sandra Boutellier ◽  
Thomas A. Lutz ◽  
Matthias Volkert ◽  
Erwin Scharrer
Keyword(s):  
Fatty Acid ◽  
Membrane Potential ◽  
Food Intake ◽  
Fatty Acid Oxidation ◽  
Intraperitoneal Injection ◽  
Acid Oxidation ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Intraportal Infusion

In former work, intraperitoneal injection of 2-mercaptoacetate (MA), an inhibitor of fatty acid oxidation, increased food intake in rats, which was attenuated by hepatic branch vagotomy, and intraportal injection of MA increased the discharge rate in hepatic vagal afferents. In the present study, we investigated, whether intraperitoneal injection or intraportal infusion of MA affects the hepatic membrane potential in rats in vivo. The liver cell membrane potential was measured in anesthetized Sprague-Dawley rats with the microelectrode technique. Intraperitoneal injection of MA at a dose of 800 μmol/kg body wt significantly decreased the hepatocyte membrane potential by 3.8 mV, whereas at a dose of 400 μmol/kg, the depolarization (1.5 mV) of the membrane was not significant. In another strain of Sprague-Dawley rats, however, MA (400 μmol/kg) produced a significant depolarization of the hepatocyte membrane 50 min (2.6 mV) and 2 h (2.9 mV) after intraperitoneal injection. Intraportal infusion of MA (400 μmol/kg) significantly depolarized the membrane 20 and 50 min after infusion by 3.3 and 4.1 mV, respectively. MA at a dose of 800 μmol/kg also depolarized the membrane (4.8 mV after 50 min). These findings in principle are consistent with the “potentiostatic” hypothesis, postulating a link between the hepatic membrane potential, afferent vagal activity, and the control of food intake.

Intraportal mercaptoacetate infusion increases afferent activity in the common hepatic vagus branch of the rat

1997 ◽  
Vol 273 (1) ◽  
pp. R442-R445 ◽  
Author(s):  
T. A. Lutz ◽  
M. Diener ◽  
E. Scharrer
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Discharge Rate ◽  
Dose Dependence ◽  
Vagal Afferents ◽  
Acid Oxidation ◽  
Feeding Response ◽  
The Common ◽  
Hepatic Fatty Acid Oxidation ◽  
Intraportal Infusion

Because dissection of the common hepatic vagus branch attenuated the feeding response to intraperitoneal injection of mercaptoacetate (MA), an inhibitor of fatty acid oxidation, in rats fed a fat-enriched diet (18% fat), the effect of MA on the discharge rate in afferents of the common hepatic vagus branch was investigated. Intraportal infusion of the Na salt of MA (200, 400, and 800 mumol/kg) in rats adapted to the 18% fat diet dose dependently increased the discharge rate in afferents of the common hepatic vagus branch, whereas NaCl and the Na salt of the structurally related compound 2-mercaptopropionate had no effect. The lowest dose of MA yielding a significant increase in the discharge rate was 400 mumol/kg. This agrees with the dose dependence of the feeding response to MA. These findings are consistent with the notion that hepatic fatty acid oxidation controls food intake by modulating the discharge rate of vagal afferents.

scholarly journals Neddylation inhibition ameliorates steatosis in NAFLD by boosting hepatic fatty acid oxidation via DEPTOR-mTOR axis

2021 ◽  
pp. 101275
Author(s):  
Marina Serrano-Maciá ◽  
Jorge Simón ◽  
Maria J. González-Rellan ◽  
Mikel Azkargorta ◽  
Naroa Goikoetxea-Usandizaga ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Acid Oxidation ◽  
Hepatic Fatty Acid ◽  
Hepatic Fatty Acid Oxidation

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.

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