Program: Abstracts - Orals, Featured Poster Presentations, and Posters
Session: MON 112-141-Hypothalamus-Pituitary Development & Biology
Monday, June 17, 2013: 1:45 PM-3:45 PM
Expo Halls ABC (Moscone Center)

Poster Board MON-140
Maria Lemini*, Xarubet Ruiz-Herrera, Montserrat Vega-Gordillo, Gonzalo Martinez de la Escalera, Yazmin Macotela and Carmen Clapp
National University of Mexico (UNAM), Querétaro, Mexico
Prolactin (PRL) may play a role in the pathophysiology of diabetes and its complications. It acts on pancreatic b cells to stimulate their proliferation, survival, and insulin production, and it inhibits retinal vascular alterations associated with diabetic retinopathy. The levels of serum PRL increase in diabetic patients and are reduced in severe diabetic retinopathy, suggesting the action of factors able to stimulate and inhibit anterior pituitary (AP)-PRL secretion during the course of the disease. Given that tumor necrosis factor-a (TNF-a) stimulates and transforming growth factor-b (TGF-b) inhibits AP-PRL expression, we investigated the influence of both factors on AP-PRL in diabetes by using the type-2 diabetes model of male rats fed a high-fat diet (HFD) and the GH4C1 lactotrope cell line. HFD-fed rats were hyperglycemic and insulin resistant. The levels of AP mRNA and circulating PRL decreased in these rats and correlated with lower and higher levels of mRNA  for TNF-a and TGF-b in the AP, respectively, suggesting that changes in TNF-a and TGF-b expression in the AP could influence PRL secretion in diabetes. Consistent with this proposal, these factors antagonized the effect of each other on GH4C1 cells. TNF-a stimulated and TGF-b inhibited PRL mRNA and protein levels in cell lysates and conditioned medium. The stimulatory and inhibitory effects of all doses of TNF-a and TGF-b were blocked by co-incubation with a single concentration of TGF-b (10 ng/ml) and TNF-a (50 ng/ml), respectively. Although NFkB is a key transcription factor mediating AP-PRL induction by TNF-a, TGF-b did not modify TNFa-induced downregulation of the NFkB inhibitor kB-a mRNA and protein, suggesting that TGF-b counteracts TNF-a stimulation by a mechanism independent of NFkB signaling. In conclusion, we suggest that altered levels of TNF-a and TGF-b in the AP modify PRL secretion in diabetes. Experiments are underway to further explore the signaling mechanisms mediating TNF-a and TGF-b  interaction.

Nothing to Disclose: ML, XR, MV, GM, YM, CC

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Sources of Research Support: CONACYT SALUD-2011-1-161594 and PAPIIT-UNAM IA200113.