scholarly journals Circulating leptin during ovine pregnancy in relation to maternal nutrition, body composition and pregnancy outcome

2001 ◽  
Vol 169 (3) ◽  
pp. 465-476 ◽  
Author(s):  
L Thomas ◽  
JM Wallace ◽  
RP Aitken ◽  
JG Mercer ◽  
P Trayhurn ◽  
...  
Keyword(s):  
Gene Expression ◽  
Body Composition ◽  
Adipose Tissue ◽  
Dietary Intake ◽  
Leptin Receptor ◽  
Maternal Nutrition ◽  
Receptor Gene ◽  
Mrna Levels ◽  
Tissue Samples ◽  
Receptor Gene Expression

This study examined the pattern of circulating leptin in age-matched sheep during adolescent pregnancy, and its relationship with maternal dietary intake, body composition and tissue expression of the leptin gene. Overfeeding the adolescent pregnant ewe results in rapid maternal growth at the expense of the placenta, leading to growth restriction in the fetus, compared with normal fed controls. Our results demonstrate that, in the adolescent ewe, overfeeding throughout pregnancy was associated with higher maternal leptin concentrations, when compared with moderately fed controls (P<0.05), with no peak in circulating leptin towards the end of pregnancy. There was a close correlation between indices of body composition and circulating leptin levels at day 104 of gestation and at term (P<0.03). Further, when the dietary intake was switched from moderate to high, or high to moderate, at day 50 of gestation, circulating leptin levels changed rapidly, in parallel with the changes in dietary intake. Leptin mRNA levels and leptin protein in perirenal adipose tissue samples, taken at day 128 of gestation, were higher in overfed dams (P<0.04), suggesting that adipose tissue was the source of the increase in circulating leptin in the overnourished ewes. Leptin protein was also detected in placenta but leptin gene expression was negligible. However, leptin receptor gene expression was detected in the ovine placenta, suggesting that the placenta is a target organ for leptin. A negative association existed between maternal circulating leptin and fetal birth weight, placental/cotyledon weight and cotyledon number. In conclusion, in this particular ovine model, hyperleptinaemia was not observed during late pregnancy. Instead, circulating leptin concentrations reflected increased levels of leptin secretion by adipose tissue primarily as a result of the increase in body fat deposition, due to overfeeding. However, there appears to be a direct effect of overfeeding, particularly in the short term. In the nutritional switch-over study, circulating leptin concentrations changed within 48 h of the change in dietary intake. The presence of leptin protein and leptin receptor gene expression in the placenta suggests that leptin could be involved in nutrient partitioning during placental and/or fetal development.

scholarly journals Effects of BDNF, T3, and corticosterone on expression of the hypothalamic obesity gene network in vivo and in vitro

2009 ◽  
Vol 296 (4) ◽  
pp. R1180-R1189 ◽  
Author(s):  
Mardi S. Byerly ◽  
Jean Simon ◽  
Elisabeth Lebihan-Duval ◽  
Michel J. Duclos ◽  
Larry A. Cogburn ◽  
...  
Keyword(s):  
Gene Expression ◽  
Body Composition ◽  
Leptin Receptor ◽  
Receptor Gene ◽  
Energy Regulation ◽  
Underlying Mechanisms ◽  
Agouti Related Protein ◽  
Receptor Gene Expression

Hypothalamic neuropeptides, neurotrophins, and systemic hormones modulate food intake and body composition. Although advances toward elucidating these interactions have been made, many aspects of the underlying mechanisms remain vague. Hypothalami from fat and lean chicken lines were assessed for differential expression of anabolic/orexigenic and catabolic/anorexigenic genes. Effects of triiodothyronine (T3), corticosterone (Cort), and brain-derived neurotrophic factor (BDNF) on expression of anabolic/orexigenic and catabolic/anorexigenic genes were tested in cultures of hypothalamic neurons. From this, we found that BDNF increased and T3 decreased gene expression for BDNF, leptin receptor (LEPR), pro-opiomelanocortin (POMC), thyrotropin releasing hormone (TRH), and agouti-related protein (AGRP). Thyroid hormone levels were manipulated during development to show that T3 inhibited BDNF, TRH, and BDNF receptor gene expression. Delivery of T3, Cort, T3 plus Cort, or vehicle in vivo continuously for 72 h indicated that Cort and T3 have overlapping roles in regulating TRH, LEPR, and POMC gene expression and that Cort and T3 regulate BDNF, neuropeptide Y, and AGRP in opposite directions. Collectively, these findings suggest that interactions between the neuropeptide BDNF and the hormones T3 and/or Cort may constitute a homeostatic mechanism that links hypothalamic energy regulation controlling body composition.

scholarly journals Characterization and Regulation of Type A Endothelin Receptor Gene Expression in Bovine Luteal Cell Types

Endocrinology ◽  
1999 ◽  
Vol 140 (5) ◽  
pp. 2110-2116 ◽  
Author(s):  
Roni Mamluk ◽  
Nitzan Levy ◽  
Bo Rueda ◽  
John S. Davis ◽  
Rina Meidan
Keyword(s):  
Gene Expression ◽  
Receptor Gene ◽  
Cell Types ◽  
Cell Populations ◽  
Mrna Levels ◽  
Factor I ◽  
Receptor Mrna ◽  
Progesterone Production ◽  
Eta Receptor ◽  
Receptor Gene Expression

Abstract Our previous studies demonstrated that endothelin-1 (ET-1), a 21-amino acid vasoconstrictor peptide, has a paracrine regulatory role in bovine corpus luteum (CL). The peptide is produced within the gland where it inhibits progesterone production by acting via the selective type A endothelin (ETA) receptors. The present study was designed to characterize ETA receptor gene expression in different ovarian cell types and its hormonal regulation. ETA receptor messenger RNA (mRNA) levels were high in follicular cells as well as in CL during luteal regression. At this latter stage, high ETA receptor expression concurred with low prostaglandin F2α receptor mRNA. The ETA receptor gene was expressed by all three major cell populations of the bovine CL; i.e. small and large luteal cells, as well as in luteal endothelial cells. Among these various cell populations, the highest ETA receptor mRNA levels were found in endothelial cells. cAMP elevating agents, forskolin and LH, suppressed ETA receptor mRNA expression in luteinized theca cells (LTC). This inhibition was dose dependent and was evident already after 24 h of incubation. In luteinized granulosa cells (LGC), 10 and 100 ng/ml of insulin-like growth factor I and insulin (only at a concentration of 2000 ng/ml) markedly decreased ETA receptor mRNA levels. In both LGC and LTC there was an inverse relationship between ETA receptor gene expression and progesterone production; insulin (in LGC) and forskolin (in LTC) enhanced progesterone production while inhibiting ETA receptor mRNA levels. Our findings may therefore suggest that, during early stages of luteinization when peak levels of both LH and insulin-like growth factor I exist, the expression of ETA receptors in the gland are suppressed. This study demonstrates physiologically relevant regulatory mechanisms controlling ETA receptor gene expression and further supports the inhibitory role of ET-1 in CL function.

LEPTIN RECEPTOR GENE EXPRESSION IN THE CHOROID PLEXUS IS INFLUENCED BY STAGE OF DEVELOPMENT AND MATERNAL STRESS IN THE GILT

2007 ◽  
Vol 77 (Suppl_1) ◽  
pp. 171-171
Author(s):  
Chad O'Gorman ◽  
Elizabeth Gonzales ◽  
Matthew Eaton ◽  
Paige Williams ◽  
Maribel Reyna ◽  
...  
Keyword(s):  
Gene Expression ◽  
Choroid Plexus ◽  
Leptin Receptor ◽  
Maternal Stress ◽  
Receptor Gene ◽  
Stage Of Development ◽  
Receptor Gene Expression

scholarly journals Modulation of glomerular endothelin and endothelin receptor gene expression in aminonucleoside-induced nephrosis.

1995 ◽  
Vol 5 (8) ◽  
pp. 1585-1590
Author(s):  
T Nakamura ◽  
I Ebihara ◽  
M Fukui ◽  
S Osada ◽  
Y Tomino ◽  
...  
Keyword(s):  
Gene Expression ◽  
Receptor Gene ◽  
Mrna Level ◽  
Experimental Period ◽  
Receptor Expression ◽  
Mrna Levels ◽  
Puromycin Aminonucleoside ◽  
Receptor Mrna ◽  
Etb Receptor ◽  
Receptor Gene Expression

This study assessed glomerular endothelin (ET)-1, ET-3, and ET-receptor A and B mRNA levels in puromycin aminonucleoside (PAN)-induced nephrosis. During the nephrotic stage, 8 days after PAN injection, ET-1 and ETB receptor mRNA were elevated by 2.8 +/- 0.8-fold (P < 0.01) and 2.4 +/- 0.9-fold (P < 0.01), respectively, as compared with controls. These mRNA levels decreased to control levels by Day 20, when the nephrosis was in remission. In contrast, glomerular ETA receptor mRNA levels did not change in PAN nephrosis or control rats during the experimental period. ET-3 mRNA was not detected in the glomeruli of PAN nephrosis or control rats. Additionally, plasma ET concentration and glomerular ET production were measured in PAN nephrosis and control rats by radio-immunoassay. Eight days after PAN injection, ET-1 levels in plasma and glomeruli were not significantly altered in rats with PAN-induced nephrosis (glomeruli, 104.68 +/- 16.46 pg/mg of protein versus 98.24 +/- 13.68 pg/mg of protein; plasma, 2.68 +/- 1.10 versus 2.52 +/- 0.98 pg/mL). The administration of methylprednisolone to PAN rats resulted in the rapid disappearance of proteinuria and partially attenuated the increased ET-1 and ETB receptor gene expression in the glomeruli. These data indicate that glomerular ET-1 and ETB receptor expression in PAN nephrosis in increased at the mRNA level and that methylprednisolone treatment results in an attenuated increase.

OMEGA-3 POLYUNSATURATED FATTY ACIDS AFFECT LEPTIN RECEPTOR GENE EXPRESSION IN PITUITARY GH4C1 CELL LINE

2009 ◽  
Vol 16 (3) ◽  
pp. 382-393 ◽  
Author(s):  
RITA DI BENEDETTO ◽  
SERAFINA SALVATI ◽  
LUCILLA ATTORRI ◽  
ANTONELLA DI BIASE
Keyword(s):  
Gene Expression ◽  
Fatty Acids ◽  
Polyunsaturated Fatty Acids ◽  
Cell Line ◽  
Leptin Receptor ◽  
Receptor Gene ◽  
Omega 3 ◽  
Receptor Gene Expression

Parathyroid hormone receptor stimulation induces human adipocyte lipolysis and browning

2021 ◽  
Vol 184 (5) ◽  
pp. 687-697
Author(s):  
Peter Breining ◽  
Steen B Pedersen ◽  
Mads Kjolby ◽  
Jacob B Hansen ◽  
Niels Jessen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Parathyroid Hormone ◽  
Receptor Gene ◽  
Receptor Expression ◽  
Whole Body ◽  
Brown Adipocyte ◽  
Cell Models ◽  
Receptor Stimulation ◽  
Receptor Gene Expression

Objective Activation of brown adipose tissue is a promising strategy to treat and prevent obesity and obesity-related disorders. Activation of uncoupling protein 1 (UCP1) leads to uncoupled respiration and dissipation of stored energy as heat. Induction of UCP1-rich adipocytes in white adipose tissue, a process known as ‘browning’, serves as an alternative strategy to increase whole body uncoupling capacity. Here, we aim to assess the association between parathyroid hormone (PTH) receptor expression and UCP1 expression in human adipose tissues and to study PTH effects on human white and brown adipocyte lipolysis and UCP1 expression. Design A descriptive study of human neck adipose tissue biopsies substantiated by an interventional study on human neck-derived adipose tissue cell models. Methods Thermogenic markers and PTH receptor gene expression are assessed in human neck adipose tissue biopsies and are related to individual health records. PTH-initiated lipolysis and thermogenic gene induction are assessed in cultured human white and brown adipocyte cell models. PTH receptor involvement is investigated by PTH receptor silencing. Results PTH receptor gene expression correlates with UCP1 gene expression in the deep-neck adipose tissue in humans. In cell models, PTH receptor stimulation increases lipolysis and stimulates gene transcription of multiple thermogenic markers. Silencing of the PTH receptor attenuates the effects of PTH indicating a direct PTH effect via this receptor. Conclusion PTH 1 receptor stimulation by PTH may play a role in human adipose tissue metabolism by affecting lipolysis and thermogenic capacity.

Prolactin Receptor Gene Expression and Foetal Adipose Tissue

1998 ◽  
Vol 10 (11) ◽  
pp. 885-890 ◽  
Author(s):  
Symonds ◽  
Phillips ◽  
Anthony ◽  
Owens ◽  
McMillen
Keyword(s):  
Gene Expression ◽  
Adipose Tissue ◽  
Receptor Gene ◽  
Prolactin Receptor ◽  
Prolactin Receptor Gene ◽  
Receptor Gene Expression
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