Evidence for conservation of dietary lipid in the rat during lactation and the immediate period after removal of the litter. Decreased oxidation of oral [1-14C]triolein

Nascimento, Cláudia Maria Oller do; Williamson, Dermot H.

doi:10.1042/bj2390233

Cited by 75 publications

(64 citation statements)

References 25 publications

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“…This is in agreement with previous studies that showed a decrease in dietary fatty oxidation during lactation in rats fed a low-fat diet (12,26). Fatty acid oxidation seems to occur preferentially in liver via PPARa, because mammary gland and adipose tissue expressed low levels of PPARa.…”

Section: Discussionsupporting

confidence: 93%

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Synthesis of long-chain polyunsaturated fatty acids in lactating mammary gland: role of Δ5 and Δ6 desaturases, SREBP-1, PPARα, and PGC-1

Rodríguez‐Cruz

Tovar

Palacios‐González

et al. 2006

Journal of Lipid Research

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The purpose of this work was to study whether rat lactating mammary gland can synthesize PUFAs through the expression of D5 and D6 desaturases (D5D and D6D), whether these enzymes are regulated by the transcription factors sterol-regulatory element binding protein 1 (SREBP-1) and peroxisome proliferator-activated receptor a (PPARa) and the coactivator peroxisome proliferator-activated receptor g coactivator 1b (PGC-1b), and whether these desaturases are regulated by the lipid concentration in the diet. The results showed that on day 12 of lactation, z35% of the linoleic acid in the diet, which is the precursor of PUFAs, is transferred to the mammary gland. There was expression of D5D and D6D in mammary gland, and it was regulated by the corn oil content in the diet. The higher the corn oil content in the diet, the lower the expression of both desaturases. Induction of D5D and D6D was associated positively with similar changes in SREBP-1 and PGC-1b. Expression of PPARa was barely detected and was not affected by the corn oil content in the diet, whereas PGC-1b expression increased as the corn oil in the diet increased. These results indicate that the lactating mammary gland has the capacity to synthesize PUFAs and can be regulated by the lipid content in the diet.-Rodriguez-Cruz, M., A. R. Tovar, B. PalaciosGonzález, M. del Prado, and N. Torres. Synthesis of longchain polyunsaturated fatty acids in lactating mammary gland: role of D5 and D6 desaturases, SREBP-1, PPARa, and PGC-1. J. Lipid Res. 2006. 47: 553-560. Supplementary key words sterol-regulatory element binding protein 1 . peroxisome proliferator-activated receptor a . peroxisome proliferator-activated receptor g coactivator 1 D5 and D6 desaturases (D5D and D6D) are microsomal enzymes that form part of a three enzyme system that includes NADH-cytochrome b 5 reductase, cytochrome b 5 , and D6D or D5D (1). Mammals are unable to synthesize long-chain polyunsaturated fatty acids (LC-PUFAs) from acetyl-CoA; thus, two PUFAs, linoleic acid (LA; 18:2 n-6) and a-linolenic acid (18:3 n-3), called essential fatty acids, must be supplied from the diet. Mammals are able to synthesize LC-PUFAs from their precursor PUFAs. Fatty acid desaturases introduce a double bond in a specific position of long-chain fatty acids and are required for the synthesis of highly unsaturated fatty acids (LC-PUFAs). The conversion of LA and a-linolenic acid to g-linolenic acid (18:3 n-6) and stearidonic acid (18:4 n-3) is determined by the enzymatic activity of D6D. After desaturation and elongation by D6D and elongase, respectively, D5D introduces another double bond at the D5 position of the 20 carbon fatty acids 20:3 n-6 and 20:4 n-3 to synthesize 20:4 n-6 (arachidonic acid; AA) and 20:5 n-3 (eicosapentanoic acid), respectively. The highly unsaturated fatty acids are mainly esterified into phospholipids and contribute to the maintenance of membrane fluidity (2). These desaturases are expressed in liver, heart, and brain and are regulated by hormonal and nutritional manipulati...

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Section: Discussionsupporting

confidence: 93%

“…The metabolic fate of an oral load of [1-14 C]LA was determined in lactating rats at day 12 of lactation as described previously (12) in each dietary treatment. Rats had free access to food during the procedure, and the litters stayed with the rats.…”

Section: Measurement Of [mentioning

confidence: 99%

Synthesis of long-chain polyunsaturated fatty acids in lactating mammary gland: role of Δ5 and Δ6 desaturases, SREBP-1, PPARα, and PGC-1

Rodríguez‐Cruz

Tovar

Palacios‐González

et al. 2006

Journal of Lipid Research

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“…The present measurements of 14CO2 production confirm the previous finding [26] (Table 3). The administration of T3 to lactating or 24 h-litter-removed rats increased 14CO2 production (by 50 and 67 % respectively), but did not increase further the high 14CO2 production in 7 days-litterremoved group (Table 3).…”

Section: C02 Production and [14c]llpid Accumulation In Liver Skelesupporting

confidence: 83%

“…The dietary lipid is conserved during lactation to provide milk fat or in the immediate period after weaning to replenish depleted adipose-tissue stores, and therefore less dietary triacylglycerols are available for oxidation [26]. The present measurements of 14CO2 production confirm the previous finding [26] (Table 3).…”

Section: C02 Production and [14c]llpid Accumulation In Liver Skelesupporting

confidence: 81%

Effects of Triiodothyronine Administration on the Disposal of Oral [1-14C]-Triolein, Lipoprotein Lipase Activity and Lipogenesis in the Rat during Lactation and on Removal of the Litter

Prado¹,

Costa²,

Williamson³

1995

Intercellular Signalling in the Mammary Gland

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“…The absorption, accumulation and oxidation of an oral dose of triolein was determined using the method of Oller do Nascimento and Williamson (1986). [Carboxy 14 C] triolein (0.33 mCi in 100 ml normal saline) was administered by intragastric intubation to NMRI mice previously administered either LMF or PBS.…”

Section: Lipid Oxidation and Accumulationmentioning

confidence: 99%

Effect of a tumour-derived lipid-mobilising factor on glucose and lipid metabolism in vivo

Russell

Tisdale

2002

Br J Cancer

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Treatment of ex-breeder male NMRI mice with lipid mobilising factor isolated from the urine of cachectic cancer patients, caused a significant increase in glucose oxidation to CO 2, compared with control mice receiving phosphate buffered saline. Glucose utilisation by various tissues was determined by the 2-deoxyglucose tracer technique and shown to be elevated in brain, heart, brown adipose tissue and gastrocnemius muscle. The tissue glucose metabolic rate was increased almost threefold in brain, accounting for the ability of lipid mobilising factor to decrease blood glucose levels. Lipid mobilising factor also increased overall lipid oxidation, as determined by the production of Loss of whole body fat is a prominent feature of cancer cachexia, with losses of up to 85% being reported (Fearon, 1992) in lung cancer patients, who had lost 30% of their pre-illness stable weight. Most studies suggest that loss of fat arises as a result of an increased lipolysis, together with increased whole body fatty acid oxidation. Thus increased plasma concentrations of glycerol, free fatty acids (FFA) and triglycerides were observed in a heterogeneous group of cancer patients with an average loss of 13% of their original body weight (Legaspi et al, 1987). Basal fatty acid turnover was elevated by 25% above that for controls, and was found to be similar to the rate observed for patients with severe burns. Lipolysis was increased by 40% in patients in whom complete triglyceride hydrolysis without re-esterification was observed, and there was a 20% increase in fatty acid oxidation.Upregulation of catabolism, rather than defects in anabolism, appear to be most important in the loss of lipid from human adipose tissue in cancer cachexia. Thus Thompson et al (1993) have shown a two-fold increase in the relative level of mRNA for triglyceride lipase, while the relative levels of mRNA for lipoprotein lipase (LPL) and fatty acid synthase were not significantly different between cancer patients and controls. This suggests that cytokines such as tumour necrosis factor-a (TNF-a), interleukin-1 (IL-1), interleukin-6 (IL-6), interferon-g (IFN-g) and leukaemiainhibitory factor (LIF), which have been proposed to decrease adipose tissue mass by decreasing synthesis of triglycerides through inhibition of LPL (Berg et al, 1994) probably play a minor role in the loss of lipid from human adipose tissue. It therefore seems more likely that lipid mobilisation in cancer cachexia can be attributed to tumour catabolic factors, such as lipid mobilising factor (LMF), which acts directly on adipose tissue with the release of FFA and glycerol in a manner similar to that of lipolytic hormones (Beck and Tisdale, 1987). LMF has been purified from the urine of patients with cancer cachexia using a combination of ion exchange, exclusion and hydrophobic interaction chromatographies (Todorov et al, 1998). Unlike polypeptide hormones stimulating lipolysis which are basic, LMF is acidic and showed homology in amino acid sequence, electrophoretic mobility and immunore...

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Evidence for conservation of dietary lipid in the rat during lactation and the immediate period after removal of the litter. Decreased oxidation of oral [1-14C]triolein

Cited by 75 publications

References 25 publications

Synthesis of long-chain polyunsaturated fatty acids in lactating mammary gland: role of Δ5 and Δ6 desaturases, SREBP-1, PPARα, and PGC-1

Synthesis of long-chain polyunsaturated fatty acids in lactating mammary gland: role of Δ5 and Δ6 desaturases, SREBP-1, PPARα, and PGC-1

Effects of Triiodothyronine Administration on the Disposal of Oral [1-14C]-Triolein, Lipoprotein Lipase Activity and Lipogenesis in the Rat during Lactation and on Removal of the Litter

Effect of a tumour-derived lipid-mobilising factor on glucose and lipid metabolism in vivo

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