scholarly journals Lipogenesis in the brain of suckling rats. Studies on the mechanism of mitochondrial-cytosolic carbon transfer

1980 ◽  
Vol 188 (1) ◽  
pp. 163-168 ◽  
Author(s):  
Tarun B. Patel ◽  
John B. Clark
Keyword(s):  
Rat Brain ◽  
Mitochondrial Membrane ◽  
Lipid Fraction ◽  
Co2 Production ◽  
Brain Lipid ◽  
Atp Citrate Lyase ◽  
Brain Lipids ◽  
Citrate Lyase ◽  
Carbon Transfer ◽  
The Brain

1. Studies on the incorporation of [3-14C]pyruvate and d-3-hydroxy[3-14C]butyrate into the brain lipid fraction by brain homogenates of the suckling (7-day-old) rat have been carried out. 2. Whereas approximately twice as much CO2 was evolved from pyruvate compared with 3-hydroxybutyrate metabolism, similar amounts of the radioactivity of these two precursors were incorporated into the lipid fraction. Furthermore, in both cases the incorporation into lipid was almost tripled when glucose (10mm) or NADPH (2.5mm) was added to the incubation media. 3. If 5mm-(—)-hydroxycitrate, an ATP–citrate lyase inhibitor, was added to the incubation the incorporation of carbon from pyruvate was inhibited to 39% of the control and from 3-hydroxybutyrate to 73% of the control, whereas CO2 production from both precursors was not affected. 4. The incorporation from pyruvate or 3-hydroxybutyrate into lipids was not affected by the presence of 10mm-glutamate in the medium (to encourage N-acetylaspartate production). However, incorporation from pyruvate was inhibited by 21% in the presence of 5mm-amino-oxyacetate (a transaminase inhibitor) and by 83% in the presence of both hydroxycitrate (5mm) and amino-oxyacetate. 5. Incorporation from 3-hydroxybutyrate into brain lipids was inhibited by 20% by amino-oxyacetate alone, but by 55% in the presence of both hydroxycitrate and amino-oxyacetate. 6. It is concluded that the mechanism of carbon transfer from pyruvate into lipids across the mitochondrial membrane in the suckling rat brain is mainly via citrate and N-acetylaspartate. 3-Hydroxybutyrate, in addition to using these routes, may also be incorporated via acetoacetate formation and transport to the cytosol.

scholarly journals Lipogenesis from ketone bodies in rat brain. Evidence for conversion of acetoacetate into acetyl-coenzyme A in the cytosol

1976 ◽  
Vol 156 (3) ◽  
pp. 603-607 ◽  
Author(s):  
M S Patel ◽  
O E Owen
Keyword(s):  
Rat Brain ◽  
Ketone Bodies ◽  
Brain Mitochondria ◽  
Atp Citrate Lyase ◽  
Acetyl Coa ◽  
Cellular Compartment ◽  
Brain Lipids ◽  
Acetyl Coenzyme A ◽  
Citrate Lyase ◽  
Old Rats

The metabolism of acetoacetate via a proposed cytosolic pathway in brain of 1-week-old rats was investigated. (-)-Hydroxycitrate, an inhibitor of ATP citrate lyase, markedly inhibited the incorporation of carbon from labelled glucose and 3-hydroxybutyrate into cerebral lipids, but had no effect on the incorporation of labelled acetate and acetoacetate into brain lipids. Similarly, n-butylmalonate and benzene-1,2,3-tricarboxylate inhibited the incorporation of labelled 3-hydroxybutyrate but not of acetoacetate into cerebral lipids. These inhibitors had no effect on the oxidation to 14CO2 of the labelled substrates used. (-)-Hydroxycitrate decreased the incorporation of 3H from 3H2O into cerebral lipids by slices metabolizing either glucose or 3-hydroxybutyrate, but not in the presence of acetoacetate. (-)-Hydroxycitrate also differentially inhibited the incorporation of [2-14C]-leucine and [U-14C]leucine into cerebral lipids. The data show that, although the acetyl moiety of acetyl-CoA generated in brain mitochondria is largely translocated as citrate from these organelles to the cytosol, a cytosolic pathway exists by which acetoacetate is converted directly into acetyl-COA in this cellular compartment.

scholarly journals Cannabis sativa and/or melatonin do not alter brain lipid but alter oxidative mechanisms in female rats

2021 ◽  
Vol 3 (1) ◽  
Author(s):  
Halimat Amin Abdulrahim ◽  
Isiaka Abdullateef Alagbonsi ◽  
Oluwasola Amuda ◽  
Noah Adavize Omeiza ◽  
Abdul-Rahuf Aderemi Feyitimi ◽  
...  
Keyword(s):  
Lipid Profile ◽  
Rat Brain ◽  
Cannabis Sativa ◽  
Density Lipoprotein ◽  
Redox Status ◽  
Female Rats ◽  
Control Group ◽  
Brain Lipid ◽  
Significant Difference ◽  
The Brain

Abstract Background Lipid profile and redox status play a role in brain (dys)functions. Cannabinoid and melatonergic systems operate in the brain and contribute to brain (patho)physiology, but their roles in the modulation of brain lipid and redox status are not well-known. We studied the effect of ethanol extract of Cannabis sativa (CS) and/or melatonin (M) on the lipid profile and anti-oxidant system of the rat brain. Methods We randomly divided twenty-four (24) female Wistar rats into 4 groups (n = 6 rats each). Group 1 (control) received distilled water mixed with DMSO. Groups II–IV received CS (2 mg/kg), M (4 mg/kg), and co-administration of CS and M (CS + M) respectively via oral gavage between 8:00 am and 10:00 am once daily for 14 days. Animals underwent 12-h fasting after the last day of treatment and sacrificed under ketamine anesthesia (20 mg/kg; i.m). The brain tissues were excised and homogenized for assay of the concentrations of the total cholesterol (TC), triacylglycerol (TG), high-density lipoprotein cholesterol (HDL-C), nitric oxide (NO), malondialdehyde (MDA), and the activities of glucose-6-phosphate dehydrogenase (G6PD), glutathione reductase (GR), glutathione peroxidase (GPx), catalase (CAT), superoxide dismutase (SOD), and acetylcholinesterase (AChE). One-way analysis of variance (ANOVA) was used to compare means across groups, followed by the least significant difference (LSD) post-hoc test. Results CS and/or M did not affect the lipid profile parameters. However, CS increased the G6PD (from 15.58 ± 1.09 to 21.02 ± 1.45 U/L; p = 0.047), GPx (from 10.47 ± 0.86 to 17.71 ± 1.04 U/L; p = 0.019), and SOD (from 0.81 ± 0.02 to 0.90 ± 0.01 μM; p = 0.007), but decreased NO (from 9.40 ± 0.51 to 6.75 ± 0.21 μM; p = 0.010) and had no effect on MDA (p = 0.905), CAT (p = 0.831), GR (p = 0.639), and AChE (p = 0.571) in comparison with the control group. M augmented the increase in G6PD (from 21.02 ± 1.45 U/L to 27.18 ± 1.81 U/L; p = 0.032) and decrease in NO (from 6.75 ± 0.21 to 4.86 ± 0.13 μM; p = 0.034) but abolished the increase in GPx (from 17.71 ± 1.04 to 8.59 ± 2.06 U/L; p = 0.006) and SOD (from 0.90 ± 0.01 to 0.70 ± 0.00 μM; p = 0.000) elicited by CS in the rat brain in comparison with the CS group. Conclusions CS and M do not alter brain lipid profile. Our data support the contention that CS elicits an anti-oxidative effect on the brain tissue and that CS + M elicits a pro-oxidant effect in rat brain.

scholarly journals Metabolic adaptations during lactogenesis. Fatty acid synthesis in rabbit mammary tissue during pregnancy and lactation

1974 ◽  
Vol 138 (3) ◽  
pp. 373-379 ◽  
Author(s):  
R. W. Mellenberger ◽  
D. E. Bauman
Keyword(s):  
Fatty Acid ◽  
Fatty Acid Synthesis ◽  
Acid Synthesis ◽  
Co2 Production ◽  
Mammary Tissue ◽  
Atp Citrate Lyase ◽  
Acetyl Coa ◽  
Citrate Lyase ◽  
Pregnancy And Lactation ◽  
Synthetic Capacity

1. Mammary tissue was obtained from rabbits at various stages of pregnancy and lactation and used for tissue-slice incubations (to measure the rate of fatty acid synthesis and CO2 production) and to determine relevant enzymic activities. A biphasic adaptation in fatty acid synthetic capacity during lactogenesis was noted. 2. The first lactogenic response occurred between day 15 and 24 of pregnancy. Over this period fatty acid synthesis (from acetate) increased 14-fold and the proportions of fatty acids synthesized changed to those characteristic of milk fat (77–86% as C8:0+C10:0 acids). 3. The second lactogenic response occurred post partum as indicated by increased rates of fatty acid synthesis and CO2 production (from acetate and glucose) and increased enzymic activities. 4. Major increases in enzymic activities between mid-pregnancy and lactation were noted for ATP citrate lyase (EC 4.1.3.8), acetyl-CoA synthetase (EC 6.2.1.1), acetyl-CoA carboxylase (EC 6.4.1.2), fatty acid synthetase, glucose 6-phosphate dehydrogenase (EC 1.1.1.49), and 6-phosphogluconate dehydrogenase (EC 1.1.1.44). Smaller increases in activity occurred with glycerol 3-phosphate dehydrogenase (EC 1.1.1.8) and NADP+–isocitrate dehydrogenase (EC 1.1.1.42) and the activity of NADP+–malate dehydrogenase (EC 1.1.1.40) was negligible at all periods tested. 5. During pregnancy and lactation there was a close temporal relationship between fatty acid synthetic capacity and the activities of ATP citrate lyase (r=0.94) and acetyl-CoA carboxylase (r=0.90).

scholarly journals Lipid membranes from naked mole-rat brain lipids are cholesterol-rich, highly phase-separated, and sensitive to amyloid-induced damage

2020 ◽  
Author(s):  
DANIEL FRANKEL ◽  
Ewan St John Smith ◽  
Kenneth Rankin ◽  
Nicolas Cenac ◽  
Matthew Davies ◽  
...  
Keyword(s):  
Rat Brain ◽  
Amyloid Beta ◽  
Lipid Membranes ◽  
Phase Behaviour ◽  
Brain Lipid ◽  
Brain Lipids ◽  
Age Related ◽  
Mole Rat ◽  
Naked Mole Rat ◽  
High Concentrations

Naked mole-rats are extraordinarily long-lived rodents that do not develop age-related neurodegenerative diseases. Remarkably, they do not accumulate amyloid plaques, even though their brains contain high concentrations of amyloid beta peptide, even from a young age Therefore, these animals offer an opportunity to investigate mechanisms of resistance against the neurotoxicity of amyloid beta aggregation. Working in this direction, here we examine the composition, phase behaviour, and amyloid beta interactions of naked mole-rat brain lipids. Relative to mouse, naked mole-rat brain lipids are rich in cholesterol and contain sphingomyelin in lower amounts and of shorter chain lengths. Proteins associated with metabolism of ceramides, sphingomyelin and ceramide receptor activity were also found to be decreased in naked mole-rat brain lysates. Correspondingly, we find that naked mole-rat brain lipid membranes exhibit a high degree of phase separation, with the liquid ordered phase occupying up to 80% of the supported lipid bilayer. These observations are consistent with the membrane pacemaker hypothesis of ageing, according to which long-living species have lipid membranes particularly resistant to oxidative damage. However, we found that exposure to amyloid beta disrupts the naked mole-rat brain lipid membranes while those formed from mouse brain lipids exhibit small, well-defined footprints, whereby the amyloid beta penetrates deeply into the lipid membranes. These results suggest that in naked mole-rats the lipid composition of cell membranes may offer neuroprotection through resistance to oxidative processes rather than through mechanical effects.

scholarly journals Incorporation of 14c-hydralazine into rat brain lipid fraction in vitro.

1980 ◽  
Vol 30 ◽  
pp. 69
Author(s):  
Shuichi Hara ◽  
Tetsuo Satoh ◽  
Haruo Kitagawa
Keyword(s):  
Rat Brain ◽  
Lipid Fraction ◽  
Brain Lipid

scholarly journals Apolipoprotein E4 disrupts the neuroprotective action of sortilin in neuronal lipid metabolism and endocannabinoid signaling

2020 ◽  
Author(s):  
Antonino Asaro ◽  
Anne-Sophie Carlo-Spiewok ◽  
Anna R. Malik ◽  
Michael Rothe ◽  
Carola G. Schipke ◽  
...  
Keyword(s):  
Lipid Metabolism ◽  
Lipid Homeostasis ◽  
Brain Lipid ◽  
Brain Lipids ◽  
Functional Studies ◽  
Amyloidogenic Processing ◽  
Apoe Receptor ◽  
Neuroprotective Actions ◽  
The Brain ◽  
Neuroprotective Action

ABSTRACTINTRODUCTIONApoE is a carrier for brain lipids and the most important genetic risk factor for Alzheimer’s disease (AD). ApoE binds the receptor sortilin which mediates uptake of apoE-bound cargo into neurons. The significance of this uptake route for brain lipid homeostasis and AD risk seen with apoE4, but not apoE3, remains unresolved.METHODSCombining neurolipidomics in patient specimens with functional studies in mouse models, we interrogated apoE isoform-specific functions for sortilin in brain lipid metabolism and AD.RESULTSSortilin directs uptake and conversion of polyunsaturated fatty acids into endocannabinoids, lipid-based neurotransmitters that act through nuclear receptors to sustain neuroprotective gene expression in the brain. This sortilin function requires apoE3, but is disrupted by binding of apoE4, impairing endocannabinoid signaling and increasing amyloidogenic processing.DISCUSSIONWe uncovered the significance of neuronal apoE receptor sortilin in facilitating neuroprotective actions of brain lipids, and its relevance for AD risk seen with apoE4.

Sign in / Sign up

Export Citation Format

Share Document