De novo sterologenesis in the intact rat

Feingold, Kenneth R.; Wiley, Millie Hughes; MacRae, Gordon; Lear, Steven R.; Moser, Arthur H.; Zsigmond, G.; Siperstein, Marvin D.

doi:10.1016/0026-0495(83)90160-9

Cited by 55 publications

(20 citation statements)

References 24 publications

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“…The incorporation of 3 H 2 O into lipids in the liver was determined as described previously. 25 - 26 The validity of our methodology for measuring lipid synthesis has been demonstrated in earlier publications.…”

Section: Lipogenesismentioning

confidence: 59%

Effect of interleukin-1 on lipid metabolism in the rat. Similarities to and differences from tumor necrosis factor.

Feingold

Soued

Adi

et al. 1991

Arterioscler Thromb

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Infection and inflammation are associated with hypertriglyceridemia, which is thought to be mediated by cytokines. Previous studies at our laboratory and others have shown that tumor necrosis factor acutely increases serum triglyceride levels primarily by stimulating hepatic lipid synthesis and secretion. The role of interleukin-1 (IL-1), a cytokine that is also secreted by stimulated macrophages and that has many actions that overlap those of tumor necrosis factor, has not been studied in depth. The present study demonstrates that IL-1, at doses similar to those that cause fever and anorexia and that stimulate adrenocorticotropic hormone secretion, rapidly increases serum triglyceride levels; this elevation persists for at least 17 hours. Serum cholesterol levels are not altered by IL-1. Neither is the clearance of triglyceride-rich lipoproteins affected by IL-1. However, hepatic triglyceride secretion, measured by the Triton WR-1339 technique, is increased in IL-1-treated animals. Accompanying this stimulation in hepatic lipid secretion is an increase in de novo fatty acid synthesis in the liver. IL-1 does not increase serum free fatty acid and glycerol levels, suggesting that IL-1 does not stimulate lipolysis in vivo. Additionally, inhibition of lipolysis does not prevent the increase in serum triglyceride levels, providing further evidence that lipolysis does not play a crucial role in the increased hepatic lipid synthesis and secretion induced by IL-1. In contrast, tumor necrosis factor increases lipolysis, which contributes to the increase in serum trigtycerides. That multiple cytokines rapidly elevate plasma triglyceride levels suggest that these changes in lipid metabolism may play an important role in the organism's response to infection and inflammation. (Arteriosclerosis and Thrombosis 1991;ll:495-500)

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Section: Lipogenesismentioning

confidence: 59%

Effect of interleukin-1 on lipid metabolism in the rat. Similarities to and differences from tumor necrosis factor.

Feingold

Soued

Adi

et al. 1991

Arterioscler Thromb

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“…This property is probably due to lipids (secreted from lamellar bodies) that fill its intercellular spaces. 2130 a major site of steroidogenesis, 20 and 15-30% of the mass of epidermal lamellar bodies is composed of sterols or their derivatives. 31 - 32 As expected from these observations, disruption of the murine epidermal permeability barrier leads to increased keratinocyte sterol synthesis during barrier recovery.…”

Section: Discussionmentioning

confidence: 99%

Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase induce reductase accumulation and altered lamellar bodies in rat forestomach keratinocytes.

Singer

Kawka

Scott

et al. 1991

Arterioscler Thromb

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Lovastatin, an inhibitor of 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) reductase and a potent hypocholesterolemic agent, induces a hyperplastic thickening of the rat forestomach mucosa after oral administration of its active form, a hydroxyacid. We studied the effects of lovastatin on the intracellular accumulation of HMG-CoA reductase immunostaining and the accompanying morphological changes in rat forestomach keratinocytes by immunofluorescence microscopy and transmission electron microscopy (TEM). Administration of lovastatin hydroxyacid induced increases in HMG-CoA reductase levels within forestomach keratinocytes that were dose and time dependent and reversible. The adjacent glandular stomach epithelium did not exhibit induction of reductase. A pharmacologically inactive epimer of lovastatin hydroxyacid did not increase keratinocyte reductase accumulation, and lovastatin lactone induced minimal forestomach reductase. TEM of forestomachs from rats given lovastatin hydroxyacid demonstrated profound alterations in epidermal lamellar bodies (organelles that transport lipids and steroids to the intercellular spaces of the stratum corneum). Treated cells lacked internal lipid lamellae and failed to secrete sheets of lipid material into the intercellular spaces of the stratum corneum. We hypothesize that sustained inhibition of HMG-CoA reductase in rat forestomach keratinocytes induces accumulation of HMG-CoA reductase and hyperplasia by inhibiting sterol synthesis, assembly of lamellar bodies, and formation of intercellular lipid sheets. {Arteriosclerosis and Thrombosis 1991;11:1156-1165)

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“…Accordingly, AQP-mediated changes in the epidermal water content also have the potential, indirectly, to influence processes involved in the maturation of the epidermal barrier. Because AQP-3, besides its water transporting capacity, also allows passage of glycerol (31) and because significant de novo lipid synthesis takes place in the basal part of the epidermis (35,36), transport of glycerol through AQP-3 might also have an impact on epidermal lipid synthesis and on the formation of the stratum corneum.…”

Section: Transepidermal Water Loss and Aquaporinsmentioning

confidence: 99%

Transepidermal Water Loss in Developing Rats: Role of Aquaporins in the Immature Skin

et al. 2003

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In the extremely preterm infant, high transepidermal water loss (TEWL) can result in severe dehydration. TEWL has been attributed to the structural properties of the epidermis but might also be influenced by mechanisms that facilitate water transport. To investigate whether aquaporins (AQP) may be involved in the extreme losses of water through immature skin, we examined the presence and cellular distributions of AQP-1 and AQP-3 in embryonic and adult rat skin by immunohistochemistry. The expression of AQP mRNA in skin was analyzed with the use of semiquantitative reverse transcription-PCR. In rat pups of different embryonic (E) and postnatal (P) ages (days), TEWL and skin hydration were measured. AQP-1 was detected in dermal capillaries, and AQP-3 was abundant in basal epidermal layers. Both AQP displayed several times higher expression in embryonic than in adult skin. TEWL was highest at embryonic day 18 (E18) (133 Ϯ 18 g/m 2 h) and lower at E20 (25 Ϯ 1 g/m 2 h) and P4 (9 Ϯ 2 g/m 2 h). Skin hydration measured as skin electrical capacitance paralleled TEWL, being highest in fetal skin (794 Ϯ 15 pF at E18) and decreasing to 109 Ϯ 11 pF at E20 and to 0 Ϯ 0 pF at P4. We conclude that, as in infants, water loss through the skin of rats decreases markedly with maturation during the perinatal period. The expression and cellular localization of the AQP are such that they might influence skin hydration and water transport and contribute to the high losses of water through the immature skin. (Pediatr Res 53: 558-565, 2003) Abbreviations TEWL, transepidermal water loss AQP, aquaporin E, embryonic P, postnatal RT, reverse transcription SEC, skin electrical capacitance Evaporation from the skin constitutes the major route of water and heat loss in extremely preterm infants early after birth (1). These losses may result in hypothermia, dehydration, and hyperosmolality, the last of which is associated with an increased risk for cerebral bleeding (2, 3). Previous observations in very preterm infants indicate that their very high loss of water from the skin, measured as transepidermal water loss (TEWL) (4, 5), is a consequence of their poorly developed epidermis (6, 7). The formation of an effective epidermal barrier, limiting water permeability, takes place in late gestation (8) and has mainly been attributed to the structural maturation of the stratum corneum and its constituents (9, 10).Aquaporin (AQP) water channels have been shown to be extensively distributed throughout different tissues and to allow rapid and regulated transcellular water transport (11,12). Only a few studies on AQP have included skin analyses. AQP-1 and -3 have been identified in adult rat skin by immunohistochemistry (13) and by RNase protection assay (14), providing support for the speculation that AQP might play a role in transepidermal water transport (15). To understand better the mechanism underlying the high TEWL in preterm infants, we investigated the pattern of distribution and gene expression of AQP-1 and -3 in rat skin at different stages of...

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De novo sterologenesis in the intact rat

Cited by 55 publications

References 24 publications

Effect of interleukin-1 on lipid metabolism in the rat. Similarities to and differences from tumor necrosis factor.

Effect of interleukin-1 on lipid metabolism in the rat. Similarities to and differences from tumor necrosis factor.

Inhibitors of 3-hydroxy-3-methylglutaryl coenzyme A reductase induce reductase accumulation and altered lamellar bodies in rat forestomach keratinocytes.

Transepidermal Water Loss in Developing Rats: Role of Aquaporins in the Immature Skin

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