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1.
J Endocrinol Invest ; 34(6): 434-8, 2011 Jun.
Article in English | MEDLINE | ID: mdl-20959720

ABSTRACT

BACKGROUND: Energy homeostasis and body weight are regulated by a highly complex network involving the brain, the digestive tract, and white adipose tissue (WAT). Knowledge about signaling pathways connecting digestive tract and WAT is limited. Gut hormone ghrelin and adipokine adiponectin are both decreased in obesity and they share a potent effect on insulin sensitivity: both adiponectin and the combination of acylated (AG) and unacylated ghrelin (UAG) improve insulin sensitivity. AIM: In the present study, we evaluated whether acute administration of UAG alone or combined with AG affects adiponectin concentrations. SUBJECTS AND METHODS: Eight morbidly obese non-diabetic subjects were treated with either UAG 200 µg, UAG 100 µg + AG 100 µg (Comb), or placebo in 3 episodes in a double blind randomized cross-over design. Study medication was administered as single iv bolus injections at 09:00 h after an overnight fast. High molecular weight (HMW) and total adiponectin, glucose, insulin, and total ghrelin and AG were measured up to 1 h after administration. RESULTS: HMW and total adiponectin concentrations did not change after administration of either UAG or Comb, nor were they different from placebo. Insulin concentrations decreased significantly after acute administration of Comb, reaching a minimum at 20 min: 58.2 ± 3.9% of baseline. CONCLUSIONS: Acute iv administration of UAG and the combination of UAG and AG in morbidly obese non-diabetic subjects without overt diabetes does not affect total or HMW adiponectin concentrations, neither directly nor indirectly by changing insulin concentrations.


Subject(s)
Adiponectin/blood , Blood Glucose/metabolism , Ghrelin/administration & dosage , Insulin/metabolism , Obesity, Morbid/blood , Acylation , Adult , Double-Blind Method , Female , Follow-Up Studies , Humans , Insulin Resistance , Male , Middle Aged , Molecular Weight , Obesity, Morbid/drug therapy , Obesity, Morbid/pathology , Prognosis
4.
Neth J Med ; 62(3): 94-6, 2004 Mar.
Article in English | MEDLINE | ID: mdl-15209475

ABSTRACT

We report the case of a 64-year-old man who presented with severe hypercalcaemia secondary to primary hyperparathyroidism. Soon after admission he developed ventricular fibrillation with no other cause than this severe hypercalcaemia. Although the occurrence of cardiac arrhythmias in hypercalcaemia is widely known, ventricular fibrillation has never been described before.


Subject(s)
Hypercalcemia/complications , Hyperparathyroidism/complications , Ventricular Fibrillation/etiology , Calcium/blood , Calcium/metabolism , Confusion , Electrocardiography , Humans , Hyperparathyroidism/metabolism , Male , Middle Aged , Risk Factors , Ventricular Fibrillation/diagnosis , Ventricular Fibrillation/metabolism
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