Endocrine Regulation of Fetal Adipose Tissue Metabolism in the Pig: Role of Thyroxine

Hausman, Dorothy B.; Hausman, Gary; Martin, Roy J.

doi:10.1159/000243981

Cited by 13 publications

(21 citation statements)

References 15 publications

(26 reference statements)

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“…Serum T4 concentrations were not increased in the hypophysectomized fetuses treated with T4 alone, compared with the untreated hypophysectomized fetuses. This finding is in contrast with those of our previous studies (3,6), where a consistent return of serum T 4 to intact values was observed in hypophysectomized fetuses treated for 3 to 14 days with T4 pellets. Serum triiodothyronine was not measured in this study because we had failed to detect measurable levels of this hormone after 20 days T4 treatment in a previous study (4).…”

Section: Resultscontrasting

confidence: 99%

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Endocrine Regulation of Fetal Adipose Tissue Metabolism in the Pig: Interaction of Porcine Growth Hormone and Thyroxine

Hausman

Martin

1999

Obesity Research

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HAUSMAN, D.B., GJ. HAUSMAN, AND RJ. MARTIN. Endocrine regulation of fetal adipose tissue metabolism in the pig: interaction of porcine growth hormone and thyroxine. Obes Res. 1999;7:76-82. Objective: This study tested the hypothesis that combined treatment of thyroxine (T 4) and growth hormone (GH) could normalize cellular and metabolic aspects of adipose tissue development of hypophysectomized fetal pigs. Research Methods and Procedures:On day 70 of gestation, pig fetuses were hypophysectomized by microcauterization or remained intact. Hypophysectomized fetuses remained untreated or were treated from day 90 to day 105 of gestation with T 4, GH, or a combination of both hormones. Results: Body weights were unaffected by hypophysectomy or hormone treatment. De novo lipogenesis in subcutaneous adipose tissue was increased 10-fold by hypophysectomy, consistent with our previous results. This increase was abolished by GH treatment in the hypophysectomized fetuses. In contrast, T 4 treatment of the hypophysectomized fetuses resulted in a 12-fold further increase in adipose tissue lipogenesis, an effect that was negated by concomitant administration of GH. Lipolytic response to isoproterenol was decreased by hypophysectomy, unaffected by GH treatment, and restored to intact values by T4 or by T4+GH treatment in the hypophysectomized fetuses. Discussion: In contrast to T 4 , GH does not influence serum insulin-like growth factor-lor adipose tissue lipolysis, but decreases lipogenesis in the fetal pig. However, replacing both T 4 and GH normalized hypophysectomized fetuses to a greater extent than either GH or T 4 alone. Thus, any

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Section: Resultscontrasting

confidence: 99%

“…Indirect evidence from a number of studies had shown that GH may antagonize lipogenesis during fetal development (2,3,(18)(19)(20)(21)(22). The results of the present study provide direct and definitive evidence that GH does antagonize or inhibit lipogenesis in the fetus.…”

Section: Discussionmentioning

confidence: 99%

Endocrine Regulation of Fetal Adipose Tissue Metabolism in the Pig: Interaction of Porcine Growth Hormone and Thyroxine

Hausman

Martin

1999

Obesity Research

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“…In vitro studies were performed as previously de scribed [5] in 25-rnl flasks containing 2.0 ml of media. After 2 h, reactions for determination of glucose oxida tion (and lipogenesis) were stopped by the addition of 0.5 ml o f 1 N LLS04 to the media and the carbon diox ide released collected for 30 min in 0.2 ml hyaminc hydroxide contained in the suspended plastic center wells.…”

Section: Metabolic Incubationsmentioning

confidence: 99%

“…Recent evidence suggests that thyroid hormones, which are under hypothalamic/pituitary control, play an important role in regulating such development [5][6][7], Previous studies in our laboratory demon strated that removal of central endocrine in fluences by hypophvsectomy of the fetal pig on day 70 of development induced fat cell hypertrophy [3] and elevations in lipoprotein lipase (LPL) activity [3], de novo lipogcnesis [4,5], and basal and insulin-stimulated glu cose metabolism [5] while decreasing fat cell number [6] and markedly impairing hor mone-stimulated lipolvsis [4,5]. More recent ly, we observed that treatment of hypophysectomized (hypox) fetal pigs with thyroxine (T4) between days 70 and 90 or 105 of gestation augmented hypophysectomy-induced eleva tions in LPL activity [6,7], lipogenic enzyme activities [6,7], and lipogenesis [5], In con trast, hormone-stimulated lipolvsis [5] and fat cell number [6,7] were normalized in hypox fetuses following 14-or 21-day treatment with T4.…”

Section: Introductionmentioning

confidence: 99%

Endocrine Regulation of Fetal Adipose Tissue Metabolism in the Pig: Ontogeny of Thyroxine Influence

Hausman

Hausman²,

Martin³

1996

Neonatology

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Our previous studies indicated that thyroxine (T₄) markedly enhanced adipose tissue development and metabolism when administered to hypophysectomized fetal pigs from days 70 to 90 of gestation. In this study, hypophysectomized (day 70) fetal pigs were implanted with T₄ pellets, and blood and adipose tissue samples were obtained upon removal on days 73, 75, 80, or 85 of gestation to examine the time course of T₄ response. T₄ treatment in hypophysectomized fetuses resulted in an elevation in serum T₄ levels by day 73 of gestation, with no further increase on day 80 or 85. Quantitative analysis of subcutaneous adipose tissue indicated that hypophysectomy per se had no influence on lipid deposition, whereas the extent of T₄-stimulated lipid deposition increased with fetal age, beginning on day 75. Glucose oxidation and lipogenesis in subcutaneous adipose tissue slices was increased by T₄ treatment in hypophysectomized fetuses by day 73 of gestation and further increased with additional time of treatment. Hypophysectomy per se induced a slight increase in lipogenesis only on days 80 and 85 of gestation. Basal lipolysis was unaffected by age, hypophysectomy, or T₄ treatment. The responsiveness to a variety of lipolytic stimuli was both accelerated and enhanced by T₄ treatment in hypophysectomized fetuses. These results indicate that the T₄ influence on adipose tissue development (1) is already apparent following only 3 days of hormone treatment in the hypophysectomized fetuses, (2) clearly precedes hypophysectomy-induced alterations in cellular and metabolic development of adipose tissue, and (3) is not mediated exclusively by serum concentrations of the hormone.

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“…HC and T 4 are inducers of preadipocyte development [16,24], while indirect [25][26][27][28][29][30][31][32] and direct evidence [22] indicates that GH antagonizes lipogenesis during fetal adipocyte differentiation. Treatment with HC or T 4 significantly increased lipid accretion, LPL and de novo lipogenesis in hypox fetuses [16,24,28,29]. T 4 enhances lipid accretion by increasing hyperplasia of adipocytes while HC enhances hypertrophy with no influence on hyperplasia [23].…”

Section: Discussionmentioning

confidence: 99%

Alterations in Fetal Adipose Tissue Leptin Expression Correlate with the Development of Adipose Tissue

Chen

Lin²,

Hausman³

et al. 2000

Neonatology

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Control pig fetuses and fetuses hypophysectomized (hypox) at 70 days of gestation were treated with hormones on day 90. At 105 days of gestation, subcutaneous adipose tissue was prepared for morphological studies, leptin Northern blot and Western blot analysis. Fetal ontogeny studies showed that leptin mRNA in adipose tissue increased with morphological development, and the highest level of leptin mRNA was observed in 105-day fetal pigs. In hypox fetuses, levels of leptin mRNA were similar to those in controls. Treatment with either hydrocortisone (HC) or thyroxine (T₄) resulted in a slight increase in leptin mRNA levels in hypox fetuses but not in intact fetuses. Supplementation with both HC and T₄ markedly stimulated leptin mRNA expression in both hypox and intact fetuses. Morphological data showed that hypox slightly enhanced lipid accretion and treatment of hypox fetuses with HC and T₄ increased lipid accretion to a greater degree than did either HC or T₄ alone. However, serum leptin levels were not influenced by age, hypox or hormone treatment. Leptin protein expression was not detected in adipose tissue of hypox or intact fetuses regardless of hormone treatment. Leptin protein was detected in adipose tissue of 7-day-old pigs and placenta. As compared to 7-day postnatal adipose tissue, placenta showed a higher level of leptin protein expression. Leptin mRNA expression in fetal adipose tissue was not correlated with body weight and organ weight. The expression of long-form leptin receptor mRNA was detected in fetal adipose tissue. Our results indicate that adipose tissue leptin may not be the main source of serum leptin in the fetus and may not be involved in general prenatal growth and development. But adipose tissue leptin may act as an autocrine or paracrine factor in the development of fetal adipose tissue.

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Endocrine Regulation of Fetal Adipose Tissue Metabolism in the Pig: Role of Thyroxine

Cited by 13 publications

References 15 publications

Endocrine Regulation of Fetal Adipose Tissue Metabolism in the Pig: Interaction of Porcine Growth Hormone and Thyroxine

Endocrine Regulation of Fetal Adipose Tissue Metabolism in the Pig: Interaction of Porcine Growth Hormone and Thyroxine

Endocrine Regulation of Fetal Adipose Tissue Metabolism in the Pig: Ontogeny of Thyroxine Influence

Alterations in Fetal Adipose Tissue Leptin Expression Correlate with the Development of Adipose Tissue

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