Carole Subramanian

University of California, Los Angeles

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Govind A. Dhopeshwarkar

University of California, Los Angeles

James F. Mead

University of California, Los Angeles

Douglas H. McConnell

Tampa General Hospital

J. F. Mead

University of California, Los Angeles

Sylvie Bony

Information Management Policies Assessment for City Transport Systems

Santhanaraman Narendran

Tamil Nadu Dr. M.G.R. Medical University

Frederic L. Hoch

Harvard University

Donald J. Jenden

University of California, Los Angeles

John R. Duncan

Materials Systems (United States)

Richard S. Jope

University of Miami

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University of California, Los Angeles

UCLA Medical Center

University of California System

Oklahoma State University Center for Health Sciences

Harvard University

Tampa General Hospital

University of South Florida

Long Beach Memorial Medical Center

Information Management Policies Assessment for City Transport Systems

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Dietary eggs and changes in plasma, liver and brain lipids of rats.

Nutrition reports international (1980)

Sylvie Bony Carole Subramanian James F. Mead Govind A. Dhopeshwarkar

Blood plasma

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Fatty acid transport into the brain

Biochimica et Biophysica Acta (BBA) - Biomembranes (1972)

Govind A. Dhopeshwarkar Carole Subramanian Douglas H. McConnell James F. Mead

10.1016/0005-2736(72)90161-7

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Citations (42)

Thyroid control over biomembranes: VI. Lipids in liver mitochondria and microsomes of hypothyroid rats

Lipids (1981)

Frederic L. Hoch Carole Subramanian Govind A. Dhopeshwarkar James F. Mead

Abstract The lipids of liver mitochondria prepared from normal rats and from rats made hypothyroid by thyroidectomy and injection with 131 INa contained similar amounts, per mg protein, of total lipids, phospholipids, neutral lipids and lipid phosphorus. Hypothyroidism caused a doubling of the relative amounts of mitochondrial cardiolipins (CL; to 20.5% of the phospholipid P) and an accompanying trend (although statistically not significant) toward decreased amounts of both phosphatidylcholines (PC) and phosphatidylserines (PS), with phosphatidylethanolamines (PE) remaining unchanged. The pattern of elevated 18∶2 fatty acyl content and depleted 20∶4 acyl groups of the mitochondrial phospholipids of hypothyroid preparations was reflected to varying degrees in the resolved phospholipids, with PC showing greater degrees of abnormality than PE, and CL showing none. Hypothyroidism produced the same abnormal pattern of fatty acyl distributions in liver microsomal total lipids as was found in the mitochondria. Hypothyroid rats, when killed 6 hr after injection of [1‐ 14 C] labeled linoleate, showed the following abnormalities: the liver incorporated less label into lipids, and converted 18∶2 not exclusively to 20∶4 (as normals do) but instead incorporated the label mainly into saturated fatty acids. These data, together with the known decrease in β‐oxidation, suggest that hypothyroidism involves possible defective step(s) in the conversion of 18∶2 to 20∶4.

Cardiolipins

Lipidology

10.1007/bf02534957

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Citations (63)

Biosynthesis of polyunsaturated fatty acids in the developing brain: I. Metabolic transformations of intracranially administered 1‐¹⁴C linolenic acid

Lipids (1976)

Govind A. Dhopeshwarkar Carole Subramanian

Abstract Thirteen‐day old rats were given intracranial injections of 1‐ 14 C linolenic acid (all cis 9,12,15 octa decatrienoic acid) and were sacrificed after 8 hr. Analysis of brain fatty acids showed that 16∶0, 18∶0, 18∶1, 18∶3, 20∶3, 20∶4, 20∶5, 22∶5, and 22∶6 were labeled. The total fatty acid methyl esters were separated into classes according to degree of unsaturation on a AgNO 3 ∶SiO 2 impregnated plate. The bands were scraped off and the eluted fatty acids were first analyzed by radiogas liquid chromatography and then subjected to reductive ozonolysis to determine double bond position. The saturated acids, 16∶0, and 18∶0, as well as the mono‐unsaturated 18∶1, must have been formed from radioactive acetate produced by β oxidation of the injected linolenate. Among the polyunsaturated fatty acids, the triene fraction was characterized and identified as 18∶3 ε3 (Δ 9,12,15 ), the starting material, and 20∶3 ω3 (Δ 11,14,17 ); the tetraene fraction was identified as 20∶4 ω3 (Δ 8,11,14,17 ); the pentaene fraction was identified as 20∶5 ω3 (Δ 5,8,11,14,17 ) and 22∶5 ω3 (Δ 7,10,13,16,19 ); and, finally, the hexaene fraction was shown to be 22∶6 ω3 (Δ 4,7,10,13,16,19 ). The biosynthesis of these ω3 family fatty acids in the brain in situ is discussed.

Lipidology

Linolenic acid

Neurochemistry

10.1007/bf02532586

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Citations (68)

Fatty acid uptake by the brain V. incorporation of [1-14c]linolenic acid into adult rat brain

Biochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism (1971)

Govind A. Dhopeshwarkar Carole Subramanian James F. Mead

Linolenic acid

10.1016/0005-2760(71)90162-7

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Citations (43)

Fatty acid uptake by the brain. V. Incorporation of (I- 14 C)linolenic acid into adult rat brain.

PubMed (1971)

Govind A. Dhopeshwarkar Carole Subramanian James F. Mead

Linolenic acid

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Lack of catabolism of brain cholesterol

Lipids (1981)

Govind A. Dhopeshwarkar Carole Subramanian

Abstract Since direct intracranial injections of precursors indicate that cholesterol is synthesized in the brain at all ages, there must be a mode of disposal also. The sterol nucleus itself is not degraded by mammalian systems but the side chain can be metabolized. [26‐ 14 C] Cholesterol was therefore injected directly into the brain of 80 to 19‐day‐old rats which were sacrificed at the end of 24 hr, 1 week and 2 weeks after injection. The results indicate that, irrespective of the interval between injection and sacrifice, all of the radioactivity was found in the free cholesterol or the cholesterol component of the sterol esters. No radioactivity was found in the fatty acids of the phospholipids. We therefore conclude that the side chain of the cholesterol does not get metabolized to propionyl CoA, which in turn, could lead to fatty acid synthesis. Radioactivity in the serum, even after 2 weeks, indicates that there must be a slow but steady exchange between the brain and the blood that would explain the route of exit for brain cholesterol.

Catabolism

Lipidology

10.1007/bf02534970

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Lipogenesis in the developing brain from intracranially administered [1‐¹⁴C] acetate and [U‐¹⁴C] glucose

Lipids (1977)

Govind A. Dhopeshwarkar Carole Subramanian

Abstract Fifteen‐day‐old rats divided into two groups were given [1‐ 14 C]acetate or [U‐ 14 C] glucose by intracranial injection and were sacrificed after 1 hr. Analysis of lipids from the two groups showed differences in the incorporation of radioactivity in the polar lipids and cholesterol. Analysis of brain fatty acid showed that whereas radioactivity from acetate was incorporated into saturated, monoand polyunsaturated fatty acids, the radioactivity from [U‐ 14 C] glucose was found only in 16∶0, 18∶0, and 18∶1. No radioactivity was found in polyunsaturated fatty acids even after concentration of this fraction by AgNO 3 :SiO 2 thin layer chromatographic method. This difference is discussed in hypothetical terms of nonhomogeneous acetyl CoA pool, formation of acetyl CoA from glucose exclusively inside the mitochondria, and activation of injected acetate to acetyl CoA.

Lipogenesis

Lipidology

10.1007/bf02570910

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INTRACRANIAL CONVERSION OF LINOLEIC ACID TO ARACHIDONIC ACID: EVIDENCE FOR LACK OF Δ⁸ DESATURASE IN THE BRAIN

Journal of Neurochemistry (1976)

Govind A. Dhopeshwarkar Carole Subramanian

Abstract Eleven‐day old rats were given intracranial injection of [1‐ 14 C]linoleic acid (all cis 9,12 octadecadienoic acid) and sacrificed after 8 h. Analysis of brain fatty acids showed that 16:0, 18:2, 20:2,20:3 and 20:4 were labeled. Separation by AgN03:Si02 TLC plates followed by reductive ozonolysis characterized thc polyunsaturated fatty acids as 18:2 (Δ9,12), 20:2 (Δ11,14), 20:3 (Δ8,11,14) and 20:4 (Δ5,8,11,14). A smaller amount of 18:3 (Δ6,9,12) was also identified. This initially suggested 20:2 (A1 1,14) as an intermediate in the optional pathway of biosynthesis of arachidonate. However, when [l‐14C]eicosadienoic acid (Δ1 1,141 itself was injected in the brain it was converted to 20:3 (Δ5,11,14) (a non‐methylene interrupted double bond system) rather than the expected 20:3 (Δ8,11,14). Only a small amount of arachidonate was formed from 20:2 (Δ11,14). Thus it was concluded that 20:2 (Δ11,14) was not an intermediate in the pathways of arachidonate biosynthesis due to lack of Δ 5 desaturase in thc brain which agrees with the findings of SPKECRER & LEE (1975) in rat liver.

10.1111/j.1471-4159.1976.tb07003.x

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Citations (47)

Metabolism of linolenic acid in developing brain: I. Incorporation of radioactivity from 1‐¹⁴C linolenic acid into brain fatty acids

Lipids (1975)

Govind A. Dhopeshwarkar Carole Subramanian

Abstract Twelve‐thirteen day old rats were given 1‐ 14 C linolenic acid by intraperitoneal injection. Fatty acids were isolated from the brains of animals sacrificed at the end of 8 and 48 hr and 15 and 45 days. Eight hr after the tracer, radioactivity was found neither in 18∶3 nor its endproduct, 22∶6, and palmitate was the most highly radioactive component. At longer intervals, 22∶6 seemed to retain much of the radioactivity, whereas palmitate showed a precipitous decline in radioactivity. Initial oxidation of linolenate and sparing of the linolenate complexed with polar lipids are discussed.

Linolenate

Linolenic acid

Lipidology

10.1007/bf02532486

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Citations (44)