Resistin Regulates Pituitary Somatotrope Cell Function through the Activation of Multiple Signaling Pathways

Rodríguez‐Pacheco, Francisca; Vázquez-Martı́nez, Rafael; Martínez-Fuentes, Antonio J.; Pulido, Marta; Gahete, Manuel D.; Vaudry, Hubert; Gracia‐Navarro, Francisco; Diéguez, Carlos; Castaño, Justo P; Malagón, Marı́a M.

doi:10.1210/en.2009-0116

Cited by 29 publications

(25 citation statements)

References 51 publications

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“…Thus, resistin could interact with different receptors depending on the tissue and cell types. Resistin activates G protein-dependent mechanism, the adenylate cyclase/cAMP/PK A pathway, the PI3-kinase/Akt pathway, the PKC, and extracellular Ca 2+ signaling through L-type voltage-sensitive Ca 2+ [3, 84–86]. …”

Section: Adipokines and Their Receptorsmentioning

confidence: 99%

Adipokine Contribution to the Pathogenesis of Osteoarthritis

Azamar-Llamas

Hernández-Molina

Ramos-Ávalos

et al. 2017

Mediators of Inflammation

132

106

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Recent studies have shown that overweight and obesity play an important role in the development of osteoarthritis (OA). However, joint overload is not the only risk factor in this disease. For instance, the presence of OA in non-weight-bearing joints such as the hand suggests that metabolic factors may also contribute to its pathogenesis. Recently, white adipose tissue (WAT) has been recognized not only as an energy reservoir but also as an important secretory organ of adipokines. In this regard, adipokines have been closely associated with obesity and also play an important role in bone and cartilage homeostasis. Furthermore, drugs such as rosuvastatin or rosiglitazone have demonstrated chondroprotective and anti-inflammatory effects in cartilage explants from patients with OA. Thus, it seems that adipokines are important factors linking obesity, adiposity, and inflammation in OA. In this review, we are focused on establishing the physiological mechanisms of adipokines on cartilage homeostasis and evaluating their role in the pathophysiology of OA based on evidence derived from experimental research as well as from clinical-epidemiological studies.

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Section: Adipokines and Their Receptorsmentioning

confidence: 99%

Adipokine Contribution to the Pathogenesis of Osteoarthritis

Azamar-Llamas

Hernández-Molina

Ramos-Ávalos

et al. 2017

Mediators of Inflammation

132

106

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“…Furthermore, at this stage, pituitary mRNA resistin levels are strongly stimulated by corticosteroids (Brown et al 2005). Administration of resistin to dispersed rat anterior pituitary cells increases GH release (Rodriguez-Pacheco et al 2009). In rat testis, resistin protein is detectable throughout postnatal development, and its mRNA is under the control of several hormones and mediators such as gonadotropins, leptin, and nutritional status (Nogueiras et al 2004).…”

Section: Introductionmentioning

confidence: 99%

Expression and effect of resistin on bovine and rat granulosa cell steroidogenesis and proliferation

Maillard¹,

Froment²,

Ramé³

et al. 2011

Reproduction

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Resistin, initially identified in adipose tissue and macrophages, was implicated in insulin resistance. Recently, its mRNA was found in hypothalamo-pituitary axis and rat testis, leading us to hypothesize that resistin may be expressed in ovary. In this study, we determined in rats and cows 1) the characterization of resistin in ovary by RT-PCR, immunoblotting, and immunohistochemistry and 2) the effects of recombinant resistin (10, 100, 333, and 667 ng/ml)GIGF1 (76 ng/ml) on steroidogenesis, proliferation, and signaling pathways of granulosa cells (GC) measured by enzyme immunoassay, [3 H]thymidine incorporation, and immunoblotting respectively. We observed that resistin mRNA and protein were present in several bovine and rat ovarian cells. Nevertheless, only bovine GC abundantly expressed resistin mRNA and protein. Resistin treatment decreased basal but not IGF1-induced progesterone (P!0.05; whatever the dose) and estradiol (P!0.005; for 10 and 333 ng/ml) production by bovine GC. In rats, resistin (10 ng/ml) increased basal and IGF1-induced progesterone secretion (P!0.0001), without effect on estradiol release. We found no effect of resistin on rat GC proliferation. Conversely, in cows, resistin increased basal proliferation (P!0.0001; for 100-667 ng/ml) and decreased IGF1-induced proliferation of GC (P!0.0001; for 10-333 ng/ml) associated with a decrease in cyclin D2 protein level (P!0.0001). Finally, resistin stimulated AKT and p38-MAPK phosphorylation in both species, ERK1/2-MAPK phosphorylation in rats and had the opposite effect on the AMPK pathway (P!0.05). In conclusion, our results show that resistin is expressed in rat and bovine ovaries. Furthermore, it can modulate GC functions in basal state or in response to IGF1 in vitro.

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“…The precise factors that mediate these inverse relationships between GH pulsatility and adiposity in humans are not yet known. Potential mechanisms include accentuation of putatively suppressive effects of free fatty acids, IGF-I, insulin, and TNF-␣ and/or attenuation of putatively stimulatory effects of adiponectin, resistin, eucortisolemia, and leptin on GH secretion (24,36,43,54). ApEn provides a model-free and scale-invariant measure of altered feedback control in interlinked systems like the GHRH/ ghrelin/somatostatin/GH axis (14,55).…”

Section: Discussionmentioning

confidence: 99%

Regulated recovery of pulsatile growth hormone secretion from negative feedback: a preclinical investigation

Veldhuis

Bowers

2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Although stimulatory (feedforward) and inhibitory (feedback) dynamics jointly control neurohormone secretion, the factors that supervise feedback restraint are poorly understood. To parse the regulation of growth hormone (GH) escape from negative feedback, 25 healthy men and women were studied eight times each during an experimental GH feedback clamp. The clamp comprised combined bolus infusion of GH or saline and continuous stimulation by saline GH-releasing hormone (GHRH), GHRP-2, or both peptides after randomly ordered supplementation with placebo (both sexes) vs. E(2) (estrogen; women) and T (testosterone; men). Endpoints were GH pulsatility and entropy (a model-free measure of feedback quenching). Gender determined recovery of pulsatile GH secretion from negative feedback in all four secretagog regimens (0.003 ≤ P ≤ 0.017 for women>men). Peptidyl secretagog controlled the mass, number, and duration of feedback-inhibited GH secretory bursts (each, P < 0.001). E(2)/T administration potentiated both pulsatile (P = 0.006) and entropic (P < 0.001) modes of GH recovery. IGF-I positively predicted the escape of GH secretory burst number and mode (P = 0.022), whereas body mass index negatively forecast GH secretory burst number and mass (P = 0.005). The composite of gender, body mass index, E(2), IGF-I, and peptidyl secretagog strongly regulates the escape of pulsatile and entropic GH secretion from autonegative feedback. The ensemble factors identified in this preclinical investigation enlarge the dynamic model of GH control in humans.

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Resistin Regulates Pituitary Somatotrope Cell Function through the Activation of Multiple Signaling Pathways

Cited by 29 publications

References 51 publications

Adipokine Contribution to the Pathogenesis of Osteoarthritis

Adipokine Contribution to the Pathogenesis of Osteoarthritis

Expression and effect of resistin on bovine and rat granulosa cell steroidogenesis and proliferation

Regulated recovery of pulsatile growth hormone secretion from negative feedback: a preclinical investigation

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