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Pctp−/− mice that lack phosphatidylcholine transfer protein (Pctp) exhibit a marked shift toward utilization of fatty acids for oxidative phosphorylation, suggesting that Pctp may regulate the entry of fatty acyl-CoAs into mitochondria. Here, we examined the influence of Pctp expression on the function and structure of brown adipose tissue (BAT), a mitochondrial-rich, oxidative tissue that mediates nonshivering thermogenesis. Consistent with increased thermogenesis, Pctp−/− mice exhibited higher core body temperatures than wild-type controls at room temperature. During a 24 h cold challenge, Pctp−/− mice defended core body temperature efficiently enough that acute, full activation of BAT thermogenic genes did not occur. Brown adipocytes lacking Pctp harbored enlarged and elongated mitochondria. Consistent with increased fatty acid utilization, brown adipocytes cultured from Pctp−/− mice exhibited higher oxygen consumption rates in response to norepinephrine. The absence of Pctp expression during brown adipogenesis in vitro altered the expression of key transcription factors, which could be corrected by adenovirus-mediated overexpression of Pctp early but not late during the differentiation. Collectively, these findings support a key role for Pctp in limiting mitochondrial oxidation of fatty acids and thus regulating adaptive thermogenesis in BAT.

ABSTRACT: Objective: We present a case and a review of relevant literature demonstrating that pituitary apoplexy rarely presents with syndrome of inappropriate antidiuretic hormone secretion (SIADH)-induced hyponatremia. We discuss management strategies, including consideration of pituitary surgery in the absence of visual disturbance if conservative management fails to control profound hyponatremia.Methods: Case report with literature review.Results: A previously healthy, 32-year-old female with a history of regular menses presented with fatigue, lethargy, severe headache, and intractable nausea with emesis. At presentation she was clinically euvolemic with intact visual fields and had hypoosmolar hyponatremia with serum sodium 109 mmol/L, serum osmolality 232 mOsm/kg, urine sodium 114 mmol/L, and urine osmolality 374 mOsm/kg. Her thyroid-stimulating hormone concentration was low normal, with a free thyroxine concentration of 0.6 ng/dL and a random serum cortisol measurement of 8.7μmg/dL. Pituitary magnetic resonance imaging revealed a macroadenoma potentially harboring a hemorrhagic component. Administration of hypertonic saline eliminated her symptoms within hours; however, she remained profoundly hyponatremic despite 72 hours of oral fluid restriction and treatment with glucocorticoids and levothyroxine. The patient underwent transsphenoidal resection, which resulted in an intraoperative rise in serum sodium and postoperative diabetes insipidus.Conclusion: Although hyponatremia as a consequence of central adrenal or thyroid insufficiency is prevalent in pituitary apoplexy, SIADH-associated hyponatremia in apoplexy is rare. If conservative approaches fail, treatment of pituitary apoplexy-induced SIADH with severe hyponatremia includes acute medical management of hyponatremia. Definitive strategies can be considered to control hyponatremia. In the few previously reported cases, SIADH was eliminated or improved by surgery; however, the risks of surgery may outweigh the benefits, as the present patient developed postoperative diabetes insipidus.Abbreviations: SIADH = syndrome of inappropriate antidiuretic hormone secretion TSH = thyroid-stimulating hormone T4 = thyroxine