To determine whether hemodynamic changes can modulate insulin action in vivo, we administered angiotensin II (A,,) to normal men under three separate, euglycemic conditions. First, in the presence of physiological hyperinsulinemia (-115 5,U/ml), infusion of A,, at rates of 2, 10, and 20 ng/min per kg caused significant elevations of blood pressure, whole-body glucose clearance, and plasma insulin concentrations in an Al, dose-dependent manner. Second, in the presence of plasma insulin concentrations that stimulate glucose transport maximally (-5,000 ,U/ml), A,, infusions increased whole-body glucose clearance without enhancing glucose extraction across the leg.Third, in the presence of basal insulin concentrations (.13 igU/ml), A,, infusions had no effect on whole-body glucose turnover or leg glucose extraction. Thus, A,, enhanced whole-body glucose utilization without directly stimulating glucose transport in a major skeletal muscle bed. To evaluate a possible hemodynamic mechanism for the effects of A,, on glucose utilization, we measured blood flow to two areas that differ in their sensitivity to insulin: the kidneys and the leg. We found that A,, redistributed blood flow away from the predominantly insulinindependent tissues of the kidney and toward the insulin-sensitive tissues of the leg during both sham and hyperinsulinemic glucose clamps. The redistribution of flow had no effect on whole-body glucose turnover when leg glucose uptake was unstimulated (sham clamps). However, when leg glucose uptake was activated by insulin, the redistribution of flow caused a net increase in whole-body glucose utilization. Our findings indicate that hemodynamic factors can modulate insulin action in vivo. Furthermore, our results suggest that variable activity of the renin-angiotensin system may contribute to inconsistencies in the association between insulin resistance and hypertension.

No abstract

Introduction: Empty Sella syndrome (ESS) is characterized by subarachnoid space herniating into the Sella turcica, causing displacement or flattening of the pituitary gland. Primary ESS has an unknown etiology, secondary ESS may be caused by trauma, infection, adenoma, ischemia, surgery, pharmacological or radiological Rx. It has been noted in 5-23% of the population, usually found incidentally in autopsies or imaging. 25% to 50% of patients have endocrine abnormalities (panhypopituitarism, DI, DM type 2, irregular menses). Headache or ophthalmological symptoms may be seen. Case summary: 55-year-old AAF with Hx of anemia, presented with lethargy and acute encephalopathy after several months of progressively worsening dizziness, muscle weakness, and fatigue. For the past few days, her appetite was poor. She also complained of cold intolerance, brittle hair, dry skin, and occasional constipation. Denied headache, blurry vision, neck pain, palpitation, previous head imaging, trauma or surgery. Remote history included an uncomplicated pregnancy; menopause occurred several years ago. Found to be hypoglycemic with blood glucose 35 mg/dl. Six D50 ampules initially improved her hypoglycemia but blood glucose quickly dropped thereafter. Placed on D5 drip; with the same results. A&O to place and person only, lacked a goiter. Lab work revealed low morning serum cortisol <1.2 mcg/dl (10-20 mcg/dl),high TSH 37.1 mU/L (0.4-4.5Mu/L), low free T4 0.2 mcg/dl (4.5-11.2 mcg/dl), low insulin 1.6 mcU/ml (4-30 mcU/dl), low C peptide 0.48 ng/ml (1.1-22 ng/ml), elevated prolactin 31 ng/ml (2-29 ng/dl), and low FSH 10 mlU/ml (26-134 mlU/ml). ACTH stimulation test revealed adrenal insufficiency. Started on IV Dexamethasone 2mg BID, hypoglycemia resolved (later weaned to prednisone 5mg BID). In view of hypothyroidism, adrenal insufficiency, and low FSH in post-menopause, hypopituitarism was suspected. MRI brain revealed empty sella without micro- or macroadenoma. Discussion & Conclusion: PES is usually asymptomatic but can present with endocrine, neurologic, or visual symptoms. A fraction of patients present with nonspecific headache, dizziness, or cranial nerve disorders. Others may have ophthalmological symptoms such as blurry or decreased vision, or mild papilledema. Though mild hyperprolactinemia and various levels of hypopituitarism have been noted, it is rare that adult patients are hospitalized for undiagnosed hypopituitarism with refractory hypoglycemia or severe hyponatremia. Panhypopituitarism is noted in only 2% of ESS patients. Our case represents a rare clinical presentation of primary ESS, with no known trauma, surgery, or ischemia. As clinicians, we should include ESS in our differential when assessing patients presenting with hypopituitarism, refractory hypoglycemia, or neurological/visual symptoms. MRI brain should be obtained if ESS is suspected. Unless otherwise noted, all abstracts presented at ENDO are embargoed until the date and time of presentation. For oral presentations, the abstracts ar...