Stimulation of lipoprotein lipase synthesis by refeeding, insulin and dexamethasone

Oliver, Jason D.; Rogers, Mark A.

doi:10.1042/bj2920525

Cited by 27 publications

(18 citation statements)

References 32 publications

(35 reference statements)

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“…We report the new observation that LPL is hormonally regulated in the lung similar to previous findings in selected other tissues, such as adipocytes (30). Immunostaining indicated localization of LPL to type II cells, with basolateral expression as required for hydrolysis of triglycerides derived from serum or adjacent fibroblasts.…”

Section: Discussionsupporting

confidence: 66%

Gene Induction during Differentiation of Human Pulmonary Type II Cells In Vitro

Wade

Guttentag

Gonzales

et al. 2006

Am J Respir Cell Mol Biol

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Mature alveolar type II cells that produce pulmonary surfactant are essential for adaptation to extrauterine life. We profiled gene expression in human fetal lung epithelial cells cultured in serumfree medium containing dexamethasone and cyclic AMP, a treatment that induces differentiation of type II cells. Microarray analysis identified 388 genes that were induced Ͼ 1.5-fold by 72 h of hormone treatment. Induced genes represented all categories of molecular function and subcellular location, with increased frequency in the categories of ionic channel, cell adhesion, surface film, lysosome, extracellular matrix, and basement membrane. In timecourse experiments, self-organizing map analysis identified a cluster of 17 genes that were slowly but highly induced (5-to ‫ف‬ 190-fold) and represented four functional categories: surfactant-related (SFTPC, SFTPA, PGC, SFTPB, LAMP3, LPL), regulatory (WIF2, IGF2, IL1RL1, NR4A2, HIF3A), metabolic (MAOA, ADH1B, SEPP1), and transport (SCNN1A, CLDN18, AQP4). Induction of both mRNA and protein for these genes, which included nine newly identified regulated genes, was confirmed, and cellular localization was determined in both fetal and postnatal tissue. Induction of lysosomal-associated membrane protein 3 required both hormones, and expression was localized to limiting membranes of lamellar bodies. Hormoneinduced differentiation of human type II cells is associated with genome-wide increased expression of genes with diverse functions. Keywords: cyclic AMP; epithelial differentiation; glucocorticoid; human fetal lung; type II cell Pulmonary type II cells have a number of known physiologic functions. During lung development, they are the progenitor cell for type I cells that constitute the gas exchange surface in alveoli. After lung injury, type II cells proliferate to repopulate the pulmonary epithelium. These cells participate in transepithelial movement of sodium and water to clear fetal lung fluid at birth and to maintain alveolar fluid homeostasis with air breathing. Type II cells produce a variety of cytokines, chemokines, and other proteins involved in the inflammatory response, as well as proteins that have either immunomodulary or antioxidant roles. The most specialized function of type II cells is the production and secretion of surfactant, the complex mixture of lipid and surfactant proteins (SPs) that maintains alveolar stability and is required for successful adaptation to extrauterine life (1-3). Differentiation of type II cells from undifferentiated precursor epithelial cells is marked by the disappearance of glycogen, which serves as a substrate for surfactant phospholipid synthesis, the formation of lamellar bodies, which are the intracellular storage sites for secreted surfactant, and expansion of the apical cell surface in the form of microvilli (4-7). A number of classes of proteins are developmentally increased during type II cell differentiation, including SPs, lipogenic enzymes, selected water and ion transporter/channels, metabolic enzymes, and structural p...

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Section: Discussionsupporting

confidence: 66%

Gene Induction during Differentiation of Human Pulmonary Type II Cells In Vitro

Wade

Guttentag

Gonzales

et al. 2006

Am J Respir Cell Mol Biol

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“…The increase in the LPL activity is consistent with previous results from Chilliard et al [3] and DiMarco et al [8], who observed that refeeding 2-day-fasted goats for 7 days or 9-day-underfed steers for [21][22][23][24][25][26][27][28][29][30][31][32][33][34][35] days increased the LPL activity by a factor of 12 (goats) and 3-7 (steers). The increase in FAS activity with refeeding is higher than the slight increase (+ 4 %) observed in the subcutaneous AT after refeeding 8-dayfasted lambs [18], but this is logical because their refeeding was only at 80 % MER, whereas our refeeding was approximately at 220 % MER.…”

supporting

confidence: 81%

“…In contrast, underfeeding and refeeding have a stimulatory and an inhibitory effect, respectively, on lipolytic enzymes [43]. In monogastric species, the responses of AT lipogenic and lipolytic enzymes to underfeeding and/or refeeding are due either to changes in mRNA levels [7,10,22,28,43] or to changes in post-translational events [9,30] Adult non-lactating non-pregnant Holstein cows (n = 4, 4-to 9-year-old) and Lacaune ewes (n = 4, 2-to 6-year-old) were used. They received a restricted diet (that provided approximately 20 % of the estimated maintenance energy requirement (MER), Inra [19]) of straw (1 kg/day) and hay (1.5 kg/day) for cows, and straw only (400-500 g/day) for ewes, for 10 or 8 days, respectively.…”

mentioning

confidence: 99%

Messenger RNAs encoding lipoprotein lipase, fatty acid synthase and hormone-sensitive lipase in the adipose tissue of underfed-refed ewes and cows

Bonnet¹,

Faulconnier²,

Fléchet³

et al. 1998

Reprod. Nutr. Dev.

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-The mechanisms involved in the nutritional regulation of genes encoding lipogenic (lipoprotein lipase (LPL) and fatty acid synthase (FAS)) and lipolytic (hormone-sensitive lipase (HSL)) enzymes were investigated by comparing the levels of the corresponding mRNAs in the adipose tissue (AT) of underfed or underfed-refed ewes and cows. Refeeding sharply increased LPL and FAS activities (19-25-and 6-8-fold, respectively) and moderately increased (2-4 fold) the activities of glucose-6-phosphate dehydrogenase (G6PDH), malic enzyme (ME) and glycerol-3-phosphate dehydrogenase (G3PDH

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“…Following DEX per se or DEX plus insulin treatment, both total mRNA and activity of LPL significantly increased in animal and human adipose tissue (58,120). Adipose tissue from prednisolone-treated patients also indicated that the increased LPL activity following glucocorticoids might be a result of inhibiting degradation of the active-dimeric form (87).…”

Section: Glucocorticoids and Peripheral Tissue Metabolismmentioning

confidence: 93%

Glucocorticoids produce whole body insulin resistance with changes in cardiac metabolism

Rodrigues

2007

American Journal of Physiology-Endocrinology and Metabolism

133

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Insulin resistance is viewed as an insufficiency in insulin action, with glucocorticoids being recognized to play a key role in its pathogenesis. With insulin resistance, metabolism in multiple organ systems such as skeletal muscle, liver, and adipose tissue is altered. These metabolic alterations are widely believed to be important factors in the morbidity and mortality of cardiovascular disease. More importantly, clinical and experimental studies have established that metabolic abnormalities in the heart per se also play a crucial role in the development of heart failure. Following glucocorticoids, glucose utilization is compromised in the heart. This attenuated glucose metabolism is associated with altered fatty acid supply, composition, and utilization. In the heart, elevated fatty acid use has been implicated in a number of metabolic, morphological, and mechanical changes and, more recently, in "lipotoxicity". In the present article, we review the action of glucocorticoids, their role in insulin resistance, and their influence in modulating peripheral and cardiac metabolism and heart disease.

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Stimulation of lipoprotein lipase synthesis by refeeding, insulin and dexamethasone

Cited by 27 publications

References 32 publications

Gene Induction during Differentiation of Human Pulmonary Type II Cells In Vitro

Gene Induction during Differentiation of Human Pulmonary Type II Cells In Vitro

Messenger RNAs encoding lipoprotein lipase, fatty acid synthase and hormone-sensitive lipase in the adipose tissue of underfed-refed ewes and cows

Glucocorticoids produce whole body insulin resistance with changes in cardiac metabolism

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