Effects of prenatal androgenization and lactation on adipose tissue metabolism in finishing single-calf heifers.

Reiling, B. A.; Drackley, J.K.; Grum, L. R.; Berger, L. L.

doi:10.2527/1997.7561504x

Cited by 12 publications

(13 citation statements)

References 38 publications

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“…Reduced insulin sensitivity of prenatal tes tosteronetreated ewes is programmed by the androgenic actions of testosterone [30]. Prenatally androgenization also exaggerates postnatal body weight gain and adipose tissue mass in heifers [31]. Prenatal androgenization in rhesus monkeys confirmed the increase in intraabdom inal fat depots in adult females that has been observed in other species [32].…”

Section: Developmental Androgenization and Programming Of Energy Homesupporting

confidence: 67%

Paracrine and intracrine contributions of androgens and estrogens to adipose tissue biology: physiopathological aspects

Waraich¹,

Mauvais-Jarvis²

2013

Hormone Molecular Biology and Clinical Investigation

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In mammals, the male and female hormones androgen and estrogen act as endocrine regulators of energy metabolism. However, adipose tissue is also a site of androgen and estrogen synthesis; androgens convert to estrogens in these tissues, and adipose tissue is also a reservoir of steroids that act locally in a paracrine and intracrine manner. Thus, in adipose tissue, the local output of sex hormones is more complex than would be suggested by routine measurement of serum hormone concentrations. This review integrates studies on the effects of androgens and estrogens in the developmental programming of adipose tissue function in early life and addresses the contributions of local androgen and estrogen metabolism on adipose tissue function in adults.

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Section: Developmental Androgenization and Programming Of Energy Homesupporting

confidence: 67%

Paracrine and intracrine contributions of androgens and estrogens to adipose tissue biology: physiopathological aspects

Waraich¹,

Mauvais-Jarvis²

2013

Hormone Molecular Biology and Clinical Investigation

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“…Supportive of the importance of the developmental window of exposure, rhesus monkeys treated with T for 15-80 days from days 40 -44 of gestation had increased total intraabdominal fat mass at 20 years of age (19), whereas those treated for only 15-35 days of gestation (29) showed no change in adiposity. Similarly, heifers exposed to excess T during the first one third of gestation had increased sc fat mass at 27 months of age (40). The variability in adiposity outcomes may stem not only from species/strain differences, timing, dosage, or quality of steroid exposure but also from the developmental time point when the adiposity measures were undertaken.…”

Section: Effects Of Prenatal T Excess On Visceral Adipositymentioning

confidence: 97%

Developmental Programming: Impact of Prenatal Testosterone Excess on Insulin Sensitivity, Adiposity, and Free Fatty Acid Profile in Postpubertal Female Sheep

et al. 2013

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Prenatal T excess causes reproductive and metabolic disruptions including insulin resistance, attributes of women with polycystic ovary syndrome. This study tested whether increases in visceral adiposity, adipocyte size, and total free fatty acids underlie the insulin resistance seen in prenatal T-treated female sheep. At approximately 16 months of age, insulin resistance and adipose tissue partitioning were determined via hyperinsulinemic euglycemic clamp and computed tomography, respectively, in control and prenatal T-treated females. Three months later, adipocyte size and free fatty acid composition were determined. Results revealed that at the postpubertal time points tested, insulin sensitivity was increased, visceral adiposity and adipocyte size in both the sc and the visceral compartments were reduced, and circulating palmitic acid was increased in prenatal T-treated females relative to controls. In parallel studies, 20-month-old prenatal T-treated females tended to have increased basal insulin to glucose ratio. Relative to earlier findings of reduced insulin sensitivity of prenatal T-treated females during early life and adulthood, these findings of increased insulin sensitivity and reduced adiposity postpubertally are suggestive of a period of developmental adaptation. The disruption observed in free fatty acid metabolism a few months later correspond to a time point when the insulin sensitivity indices of prenatal T-treated animals appear to shift toward insulin resistance. In summary, current findings of improved insulin sensitivity and reduced visceral adiposity in postpubertal prenatal T-treated sheep relative to our earlier findings of reduced insulin sensitivity during early postnatal life and adulthood are indicative of a period of developmental adaptation.

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“…Prenatal androgenization increases visceral adiposity in female non-human primates (1), heifers (2) and rats (3). Neonatal exposure to testosterone increases visceral fat deposition in adult female rats (4, 5, 6).…”

Section: Introductionmentioning

confidence: 99%

Central mechanisms of adiposity in adult female mice with androgen excess

Nohara

Laque

Allard

et al. 2014

Obesity

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Objective Androgen excess in women is associated with visceral adiposity. However, little is known on the mechanism through which androgen promotes visceral fat accumulation. Design and Methods To address this issue, we exposed female mice to chronic androgen excess using 5α-dihydrotestosterone (DHT) and studied the regulation of energy homeostasis. Results DHT induced a leptin failure to decrease body weight associated with visceral adiposity but without alterations in leptin anorectic action. This paralleled leptin’s failure to upregulate brown adipose tissue expression of uncoupling protein-1, associated with decreased energy expenditure. DHT decreased hypothalamic proopiomelanocortin (pomc) mRNA expression and increased POMC intensity in neuronal bodies of the arcuate nucleus while simultaneously decreasing the intensity of POMC projections to the dorsomedial hypothalamus (DMH). This was associated with a failure of the melanocortin 4 receptor agonist melanotan-II to suppress body weight. Conclusion Taken together, these data indicate that androgen excess promotes visceral adiposity with reduced POMC neuronal innervation in the DMH, reduced energy expenditure but without hyperphagia.

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Effects of prenatal androgenization and lactation on adipose tissue metabolism in finishing single-calf heifers.

Cited by 12 publications

References 38 publications

Paracrine and intracrine contributions of androgens and estrogens to adipose tissue biology: physiopathological aspects

Paracrine and intracrine contributions of androgens and estrogens to adipose tissue biology: physiopathological aspects

Developmental Programming: Impact of Prenatal Testosterone Excess on Insulin Sensitivity, Adiposity, and Free Fatty Acid Profile in Postpubertal Female Sheep

Central mechanisms of adiposity in adult female mice with androgen excess

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