Lipid and fatty acid profiles in the brain, liver, and stomach contents of neonatal rats: effects of hypoxia

Bruder, Eric D.; Lee, Ping C.; Raff, Hershel

doi:10.1152/ajpendo.00362.2004

Cited by 12 publications

(14 citation statements)

References 40 publications

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“…Another cave at that is inherent in this experimental model is that dams were exposed to hypoxia and, therefore, that some of the effects observed in pups could be due to maternal factors such as lactation and milk composition. We have previously demonstrated minor changes in milk composition in this model ( 29 ). Furthermore, levels of ionized calcium, intact PTH, 25-hydroxy-vitamin D, osteocalcin, and total calcium and phosphorus in hypoxic nursing pups are not altered by hypoxia indicating normal absorption of calcium and vitamin D from milk ( 30 ).…”

Section: Discussionmentioning

confidence: 71%

Adiponectin and Resistin in the Neonatal Rat: Effects of Dexamethasone and Hypoxia

Raff

Bruder

2006

ENDO

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Hypoxia is a common neonatal stress that induces insulin resistance and a decrease in body weight gain. Dexamethasone is often used to treat neonatal cardiopulmonary disease, and also leads to insulin resistance and a decrease in body weight gain. The current study addressed the hypothesis that serum concentrations of the adipokines adiponectin and/or resistin are altered during hypoxia and/or dexamethasone therapy in neonatal rats. Rat pups with their lactating dams were exposed to hypoxia (11% O 2 ) from birth and treated with a tapering regimen of dexamethasone from postnatal day (PD) 3-6. Serum adiponectin and resistin were measured on PD7. Hypoxia and dexamethasone independently decreased body weight gain and increased adiponectin levels. The combination of hypoxia and dexamethasone did not further increase adiponectin. Dexamethasone caused a small increase in resistin in normoxic pups, which may facilitate the hyperinsulemic-normoglycemic state we previously described. We also conclude that adiponectin is increased during hypoxia in response to a decrease in the sensitivity to insulin.

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Section: Discussionmentioning

confidence: 71%

Adiponectin and Resistin in the Neonatal Rat: Effects of Dexamethasone and Hypoxia

Raff

Bruder

2006

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“…For example, modified low-density lipoprotein (LDL), such as oxidized LDL, is formed after cerebral ischemia and could activate CD36 (Uno et al, 2003;Shie et al, 2004;Vibo et al, 2007). In addition, hypoxia has been reported to produce diacylglyceride, a CD36 ligand that is involved in inflammatory signaling via toll-like receptors 2/6 (TLR2/6; see below) (Bruder et al, 2005;Hoebe et al, 2005). Therefore, ischemia has the potential of generating several CD36 ligands that could play a role in postischemic CD36 signaling.…”

Section: Discussionmentioning

confidence: 99%

Nuclear Factor-κB Activation and Postischemic Inflammation Are Suppressed in CD36-Null Mice after Middle Cerebral Artery Occlusion

Kunz¹,

Abe²,

Hochrainer³

et al. 2008

J. Neurosci.

102

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CD36, a class-B scavenger receptor involved in multiple functions, including inflammatory signaling, may also contribute to ischemic brain injury through yet unidentified mechanisms. We investigated whether CD36 participates in the molecular events underlying the inflammatory reaction that accompanies cerebral ischemia and may contribute to the tissue damage. We found that activation of nuclear factor-B, a transcription factor that coordinates postischemic gene expression, is attenuated in CD36-null mice subjected to middle cerebral artery occlusion. The infiltration of neutrophils and the glial reaction induced by cerebral ischemia were suppressed. Treatment with an inhibitor of inducible nitric oxide synthase, an enzyme that contributes to the tissue damage, reduced ischemic brain injury in wild-type mice, but not in CD36 nulls. In contrast to cerebral ischemia, the molecular and cellular inflammatory changes induced by intracerebroventricular injection of interleukin-1␤ were not attenuated in CD36-null mice. The findings unveil a novel role of CD36 in early molecular events leading to nuclear factor-B activation and postischemic inflammation. Inhibition of CD36 signaling may be a valuable therapeutic approach to counteract the deleterious effects of postischemic inflammation.

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“…With regard to metabolism in the liver, HIF-1 regulates the expression of glucose transporters as well as glycolytic enzymes and is thought to contribute to the glycolytic phenotype of hepatocellular carcinomas (11,36,46). In addition, recent studies have suggested a role for HIF in the regulation of hepatic lipid metabolism; however, the contributions of HIF-1 and/or HIF-2 in this process remain unclear (1,10,17,49).…”

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confidence: 99%

Hypoxia-Inducible Factor 2 Regulates Hepatic Lipid Metabolism

Rankin

Rha

Selak

et al. 2009

Molecular and Cellular Biology

285

280

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In mammals, the liver integrates nutrient uptake and delivery of carbohydrates and lipids to peripheral tissues to control overall energy balance. Hepatocytes maintain metabolic homeostasis by coordinating gene expression programs in response to dietary and systemic signals. Hepatic tissue oxygenation is an important systemic signal that contributes to normal hepatocyte function as well as disease. Hypoxia-inducible factors 1 and 2 (HIF-1 and HIF-2, respectively) are oxygen-sensitive heterodimeric transcription factors, which act as key mediators of cellular adaptation to low oxygen. Previously, we have shown that HIF-2 plays an important role in both physiologic and pathophysiologic processes in the liver. HIF-2 is essential for normal fetal EPO production and erythropoiesis, while constitutive HIF-2 activity in the adult results in polycythemia and vascular tumorigenesis. Here we report a novel role for HIF-2 in regulating hepatic lipid metabolism. We found that constitutive activation of HIF-2 in the adult results in the development of severe hepatic steatosis associated with impaired fatty acid ␤-oxidation, decreased lipogenic gene expression, and increased lipid storage capacity. These findings demonstrate that HIF-2 functions as an important regulator of hepatic lipid metabolism and identify HIF-2 as a potential target for the treatment of fatty liver disease.The liver plays a central role in maintaining overall organism energy balance by controlling carbohydrate and lipid metabolism. Hepatocytes coordinate these processes by regulating gene expression programs in response to dietary signals from the portal vein and systemic signals from the hepatic artery. Oxygen is an important systemic signal that modulates metabolic activities and disease in the liver. Under physiologic conditions, an oxygen gradient is established in the liver such that the partial pressure of oxygen in periportal blood is 60 to 65 mm Hg and in the perivenous blood is 30 to 35 mm Hg (17). This oxygen gradient is important for the zonation of metabolic activity in the liver. Because oxygen is an essential electron acceptor for oxidative metabolism, hepatocytes that perform glucose or fatty acid oxidation are located in the aerobic periportal zone, whereas oxygen-independent metabolic functions such as glucose uptake, glycolysis, and fatty acid synthesis are predominately performed by perivenous hepatocytes (16). Patients who experience perivenous hypoxia as a result of heart failure, obstructive sleep apnea, or excessive alcohol use can develop chronic liver injury characterized by steatosis and inflammation (17). Therefore, it is critical that oxygen-signaling pathways in hepatocytes are appropriately integrated into adaptive and/or maladaptive liver injury responses.Hypoxia-inducible transcription factors (HIFs) are important components of the cellular oxygen-signaling pathway. In response to low oxygen tensions, HIFs facilitate both oxygen delivery and adaptation to oxygen deprivation by regulating the expression of genes that are i...

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Lipid and fatty acid profiles in the brain, liver, and stomach contents of neonatal rats: effects of hypoxia

Cited by 12 publications

References 40 publications

Adiponectin and Resistin in the Neonatal Rat: Effects of Dexamethasone and Hypoxia

Adiponectin and Resistin in the Neonatal Rat: Effects of Dexamethasone and Hypoxia

Nuclear Factor-κB Activation and Postischemic Inflammation Are Suppressed in CD36-Null Mice after Middle Cerebral Artery Occlusion

Hypoxia-Inducible Factor 2 Regulates Hepatic Lipid Metabolism

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