Mating behavior is controlled by acute changes in metabolic fuels

2002 ◽  
Vol 282 (3) ◽  
pp. R782-R790 ◽  
Author(s):  
Jennifer L. Temple ◽  
Jill E. Schneider ◽  
Deanna K. Scott ◽  
Alexander Korutz ◽  
Emilie F. Rissman
Keyword(s):  
Fatty Acid ◽  
Blood Glucose ◽  
Mating Behavior ◽  
Fatty Acid Oxidation ◽  
Food Restriction ◽  
Ketone Bodies ◽  
Acid Oxidation ◽  
Glucose Levels ◽  
Ad Libitum ◽  
Feeding Bout

Mild food restriction for 48 h inhibits mating behavior in female musk shrews ( Suncus murinus). However, mating behavior is restored after a 90-min feeding bout. In this series of experiments, we examined the role of metabolic fuels in this behavioral restoration. First, drugs reported to block glycolysis or fatty acid oxidation were given 2 h before mating. Both treatments inhibited mating in food-restricted females that were refed after treatment. Blood glucose levels were assessed in females that were fed ad libitum, food restricted, or food restricted and refed for 90 min. Food restriction significantly lowered blood glucose compared with ad libitum feeding or food restriction in combination with 90 min of refeeding. However, neither glucose nor fat alone could substitute for food and promote mating behavior in food-restricted females. In addition, analysis of ketone bodies and body composition in females demonstrated low or undetectable levels of these energy substrates. Our data suggest that musk shrews have relatively little stored energy. Therefore, female musk shrews rely on continuous food intake and monitor multiple cues acutely, including glucose availability and fatty acid oxidation. This ensures that mating does not occur when adequate energy is unavailable.

scholarly journals The effects of inhibition of fatty acid oxidation in suckling newborn rats

1977 ◽  
Vol 166 (3) ◽  
pp. 631-634 ◽  
Author(s):  
J P Pégorier ◽  
P Ferré ◽  
J Girard
Keyword(s):  
Fatty Acid ◽  
Blood Glucose ◽  
Fatty Acid Oxidation ◽  
Glucose Utilization ◽  
Ketone Bodies ◽  
Normal Blood ◽  
Acid Oxidation ◽  
Newborn Rats ◽  
Normal Blood Glucose ◽  
Blood Ketone Bodies

Inhibition of fatty acid oxidation with pent-4-enoate in suckling newborn rats caused a fall in blood [glucose] and blood [ketone bodies] and inhibition of gluconeogenesis from lactate. Glucose utilization was not increased in newborn rats injected with pent-4-enoate. Active fatty acid oxidation appears to be essential to support gluconeogenesis and to maintain normal blood [glucose] in suckling newborn rats.

Control of food intake by fatty acid oxidation

1986 ◽  
Vol 250 (6) ◽  
pp. R1003-R1006 ◽  
Author(s):  
E. Scharrer ◽  
W. Langhans
Keyword(s):  
Fatty Acid ◽  
Blood Glucose ◽  
Food Intake ◽  
Fatty Acid Oxidation ◽  
Ketone Bodies ◽  
Acid Oxidation ◽  
Dark Phase ◽  
Fat Level ◽  
Plasma Ffa

The role of fatty acid oxidation in the control of food intake was studied using mercaptoacetate (MA), an inhibitor of fatty acid oxidation. Food intake, plasma free fatty acids (FFA) and ketone bodies, and blood glucose were measured. Rats were fed either a low-fat (LF, 3.33% fat) or a medium-fat (MF, 18% fat) diet. At the onset of the dark phase of the lighting cycle, MA did not affect food intake in LF rats but increased it 74% in MF rats in comparison to control. Four hours after the injection the effect of MA on food intake disappeared. In the middle of the bright phase of the lighting cycle, MA increased food intake in MF rats approximately 120% up to 6 h postinjection. After MA, plasma FFA concentration was elevated, and plasma 3-hydroxybutyrate concentration was lowered, indicating that fatty acid oxidation had been successfully reduced. MA did not affect blood glucose. These results indicate fatty acid oxidation is involved in the control of food intake, at least when the dietary fat level is relatively high.

Site of action of putative lipostatic factor: hypothalamic metabolism of parabiotic rats

1989 ◽  
Vol 257 (1) ◽  
pp. R224-R228
Author(s):  
T. R. Kasser ◽  
R. B. Harris ◽  
R. J. Martin
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Caloric Intake ◽  
Metabolic Adaptation ◽  
Acid Oxidation ◽  
Gamma Aminobutyric Acid ◽  
Glucose Flux ◽  
Site Of Action ◽  
Net Flux ◽  
Ad Libitum

Studies were conducted to determine whether metabolic adaptation occurred in the hypothalamus of overfed parabiotic rats and their partners to distinguish between the adaptations caused by increased caloric intake and those caused by the production of a "lipostatic factor." The induction of overfed obesity in one parabiotic partner was employed to test the hypothesis that a putative lipostatic factor produced in the obese parabiotic elicited the hypophagic-lipid-mobilizing effect observed in the lean parabiotic via alterations in hypothalamic fatty acid and glucose metabolism. Fatty acid oxidation in the ventrolateral hypothalamus (VLH) of overfed parabiotic rats and their partners was lower than in ad libitum parabiotic rats. Net flux of glucose through the VLH gamma-aminobutyric acid (GABA) shunt was elevated in overfed parabiotic rats compared with the net flux observed in their partners and ad libitum parabiotic rats, the levels being similar in these last two groups. Net flux of glucose through the ventromedial hypothalamic (VMH) pentose shunt in overfed parabiotic rats and their partners was elevated relative to ad libitum parabiotic rats. The putative lipostatic factor may act to regulate energy balance through modification of VLH fatty acid oxidation and/or glucose flux via the VMH pentose shunt.

Disorders of carbohydrate metabolism

2011 ◽  
pp. 1677-1683
Author(s):  
Robin H. Lachmann
Keyword(s):  
Fatty Acid ◽  
Carbohydrate Metabolism ◽  
Fatty Acid Oxidation ◽  
Ketone Bodies ◽  
Glycogen Synthesis ◽  
Acid Oxidation ◽  
Defence Mechanisms ◽  
Glucose Homoeostasis ◽  
Alternative Sources ◽  
Glycogen Stores

Many disorders of carbohydrate metabolism are characterized by hypoglycaemia and attacks of neuroglycopenia. Hypoglycaemia can also be caused by disorders affecting the use of other fuels, such as those producing fatty acids and ketone bodies which are important alternative sources of energy. Thus when investigating a patient with hypoglycaemia it is necessary to investigate not only pathways that provide glucose directly, but also those which spare glucose utilization and thus provide defence mechanisms when carbohydrate energy sources become depleted. The defence mechanisms that are activated during fasting to preserve blood glucose are: ◆ glycogenolysis—glucose liberation from glycogen degradation ◆ gluconeogenesis—glucose production from pyruvate/lactate and from noncarbohydrate sources such as glucogenic amino acids and glycerol ◆ fatty acid β‎-oxidation—catabolism of triglycerides to acetyl-CoA and ketone bodies The interrelation between these glucose generating pathways is shown in Fig. 12.3.1.1. Although there is much overlap, the activation of these defence mechanisms during fasting is sequential. The first defence mechanism, glycogenolysis, is exhausted within 8–12 h of fasting. The second and third defence mechanisms provide glucose once glycogen stores have been depleted. In a patient with glycogen storage disease (GSD) where glycogenolysis is blocked, gluconeogenesis and fatty acid oxidation are activated immediately on fasting and can only maintain normoglycaemia for a few hours. In patients with defects affecting gluconeogenesis or fatty acid oxidation, hypoglycaemia does not occur until glycogen stores have been depleted. When more than one pathway is affected, as in GSD I, where neither glycogenolysis nor gluconeogenesis can release glucose into the circulation, patients can be entirely dependent on oral carbohydrate intake to maintain normoglycaemia. These pathways are also susceptible to hormonal influences. Insulin in particular inhibits all three pathways and stimulates some enzymes of the reverse pathways: glycogen synthesis, glycolysis, and fatty acid synthesis. Therefore hyperinsulinaemia of whatever cause leads to severe hypoglycaemia which is resistant to treatment. Other hormones, such as glucagon, adrenaline, and growth hormone, also activate some enzymes of glucose homoeostasis, though less markedly. This is discussed elsewhere. The metabolism of the other monosaccharides, galactose and fructose, is connected with that of glucose. As well as causing hypoglycaemia, inherited defects that affect the metabolism of these sugars lead to the accumulation of toxic metabolites which also contribute to pathology (see below).

KETONE BODY METABOLISM IN NUTRITIONAL MYOPATHY

1964 ◽  
Vol 42 (8) ◽  
pp. 1153-1160 ◽  
Author(s):  
K. J. Jenkins
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Ketone Body ◽  
Ketone Bodies ◽  
Pectoral Muscle ◽  
Acid Oxidation ◽  
Dystrophic Muscle ◽  
Liver Homogenates ◽  
Ketone Body Metabolism

A study was conducted on the metabolism of ketone bodies in tissue preparations from normal and dystrophic chicks. The data indicated that the production of ketone bodies in liver homogenates, as a result of fatty acid oxidation, was not markedly altered by development of the dystrophic condition. Whereas acetoacetate was oxidized by normal and degenerative pectoral muscle to approximately the same extent, utilization of β-hydroxybutyrate in dystrophic muscle was markedly poorer. In view of present concepts of the reactions involved in the metabolism of ketone bodies the results suggest that in the chick myopathy the conversion of β-hydroxybutyrate to acetoacetate may be impaired.

scholarly journals The SGLT2 inhibitor canagliflozin suppresses lipid synthesis and interleukin-1 beta in ApoE deficient mice

2020 ◽  
Vol 477 (12) ◽  
pp. 2347-2361
Author(s):  
Emily A. Day ◽  
Rebecca J. Ford ◽  
Jessie H. Lu ◽  
Rachel Lu ◽  
Lucie Lundenberg ◽  
...  
Keyword(s):  
Fatty Acid ◽  
Blood Glucose ◽  
Energy Expenditure ◽  
Fatty Acid Oxidation ◽  
Liver Lipid ◽  
Sglt2 Inhibitor ◽  
Lipid Synthesis ◽  
Metabolic Energy ◽  
Metabolic Effects ◽  
Acid Oxidation

Sodium-glucose cotransporter 2 inhibitors such as canagliflozin lower blood glucose and reduce cardiovascular events in people with type 2 diabetes through mechanisms that are not fully understood. Canagliflozin has been shown to increase the activity of the AMP-activated protein kinase (AMPK), a metabolic energy sensor important for increasing fatty acid oxidation and energy expenditure and suppressing lipogenesis and inflammation, but whether AMPK activation is important for mediating some of the beneficial metabolic effects of canagliflozin has not been determined. We, therefore, evaluated the effects of canagliflozin in female ApoE−/− and ApoE−/−AMPK β1−/− mice fed a western diet. Canagliflozin increased fatty acid oxidation and energy expenditure and lowered adiposity, blood glucose and the respiratory exchange ratio independently of AMPK β1. Canagliflozin also suppressed liver lipid synthesis and the expression of ATP-citrate lyase, acetyl-CoA carboxylase and sterol response element-binding protein 1c independently of AMPK β1. Canagliflozin lowered circulating IL-1β and studies in bone marrow-derived macrophages indicated that in contrast with the metabolic adaptations, this effect required AMPK β1. Canagliflozin had no effect on the size of atherosclerotic plaques in either ApoE−/− and ApoE−/−AMPK β1−/− mice. Future studies investigating whether reductions in liver lipid synthesis and macrophage IL-1β are important for the cardioprotective effects of canagliflozin warrant further investigation.

scholarly journals Biochemical Markers for the Diagnosis of Mitochondrial Fatty Acid Oxidation Diseases

2021 ◽  
Vol 10 (21) ◽  
pp. 4855
Author(s):  
Pedro Ruiz-Sala ◽  
Luis Peña-Quintana
Keyword(s):  
Fatty Acid ◽  
Newborn Screening ◽  
Fatty Acid Oxidation ◽  
Biochemical Markers ◽  
Ketone Bodies ◽  
Clinical Situation ◽  
Acid Oxidation ◽  
Mitochondrial Fatty Acid Oxidation ◽  
Screening Programs ◽  
Mitochondrial Fatty Acid

Mitochondrial fatty acid β-oxidation (FAO) contributes a large proportion to the body’s energy needs in fasting and in situations of metabolic stress. Most tissues use energy from fatty acids, particularly the heart, skeletal muscle and the liver. In the brain, ketone bodies formed from FAO in the liver are used as the main source of energy. The mitochondrial fatty acid oxidation disorders (FAODs), which include the carnitine system defects, constitute a group of diseases with several types and subtypes and with variable clinical spectrum and prognosis, from paucisymptomatic cases to more severe affectations, with a 5% rate of sudden death in childhood, and with fasting hypoketotic hypoglycemia frequently occurring. The implementation of newborn screening programs has resulted in new challenges in diagnosis, with the detection of new phenotypes as well as carriers and false positive cases. In this article, a review of the biochemical markers used for the diagnosis of FAODs is presented. The analysis of acylcarnitines by MS/MS contributes to improving the biochemical diagnosis, both in affected patients and in newborn screening, but acylglycines, organic acids, and other metabolites are also reported. Moreover, this review recommends caution, and outlines the differences in the interpretation of the biomarkers depending on age, clinical situation and types of samples or techniques.

Competition between palmitate and ketone bodies as fuels for the heart: study with positron emission tomography

1993 ◽  
Vol 264 (3) ◽  
pp. H701-H707 ◽  
Author(s):  
J. L. Vanoverschelde ◽  
W. Wijns ◽  
J. Kolanowski ◽  
A. Bol ◽  
P. M. Decoster ◽  
...  
Keyword(s):  
Positron Emission Tomography ◽  
Fatty Acid ◽  
Fatty Acid Oxidation ◽  
Ketone Bodies ◽  
Emission Tomography ◽  
Acid Oxidation ◽  
Rapid Phase ◽  
Positron Emission ◽  
Myocardial Clearance

To test the ability of ketone bodies to inhibit myocardial fatty acid oxidation in vivo, the myocardial clearance kinetics of [1–11C]palmitate was assessed with positron emission tomography in six fasted volunteers and six instrumented dogs, studied repeatedly before and during infusion of 3-hydroxybutyrate (17 mumol.kg-1 x min-1). With the use of multiexponential fitting of tissue time-activity curves, the size, half time (T1/2), and index of the early rapid phase of 11C myocardial clearance, reflecting palmitate oxidation, were calculated. In humans, the relative size (-28%, P < 0.001) and index (-37%, P < 0.01) of the early rapid phase decreased significantly during infusion of 3-hydroxybutyrate, consistent with decreased fatty acid oxidation. Paradoxically, T1/2 decreased from 10.1 +/- 1.6 to 7.4 +/- 1.1 min (P < 0.01). To elucidate possible mechanisms, multiple coronary arteriovenous samples were obtained from the dogs to assess the efflux of oxidized and nonmetabolized tracer. Infusion of 3-hydroxybutyrate resulted in decreased myocardial [11C]CO2 production (-40%, P < 0.05) and reduced palmitate retention (-38%, P < 0.05). In three dogs, the arteriovenous difference in radiolabeled palmitate became negative 10 min after injection, indicating backdiffusion of nonmetabolized tracer from the myocardium. Thus a steady-state infusion of 3-hydroxybutyrate, resulting in physiological plasma levels, alters [1-11C]palmitate kinetics in vivo by decreasing myocardial long-chain fatty acid oxidation and by increasing backdiffusion of nonmetabolized tracer.

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