Lanreotide is a somatostatin analog which possesses antidiuretic activity in the rat. To determine whether vasopressin participates in the antidiuretic response to lanreotide, experiments were performed with diabetes insipidus (DI) rates homozygous for vasopressin deficiency. Lanreotide significantly increased urine osmolality and decreased urine volume and free water clearance during the 2-h period after injecting 400 microgram/kg s.c. in 12 awake Wistar-Kyoto rats that were undergoing water diuresis. Although lanreotide decreased serum growth hormone levels (24.2 +/- 6.1 vs. 0.9 +/- 0.1 ng/ml, P < .01), administration of recombinant human growth hormone (1 mg/kg s.c.) did not affect the renal response. Lanreotide (200 microgram/kg s.c.) also significantly increased urine osmolality and free water reabsorption and tended to decrease urine volume in 15 water-loaded Long-Evans rats. In contrast, lanreotide (200 or 400 microgram/kg s.c.) did not affect urine osmolality, urine volume or free water clearance when administered acutely or chronically to DI rats. These results suggest that vasopressin plays a role in the renal response to lanreotide in the rat
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Pituitary
December 2024
Institute of Endocrine and Metabolic Sciences, San Raffaele Vita-Salute University and IRCCS San Raffaele Hospital, Milan, Italy.
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College of Medicine, Alfaisal University, Riyadh 11211, Saudi Arabia.
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Endocrinology Unit, Department of Clinical and Molecular Medicine, Sant'Andrea Hospital, European Neuroendocrine Tumor Society (ENETS) Center of Excellence, Sapienza University of Rome, Rome, Italy.
Neuroendocrine neoplasms (NENs) originating in the gastroenteropancreatic (GEP) tract are rare tumors often associated with significant metabolic disturbances and nutritional challenges. This review explores the intricate relationship between nutritional status and the development, progression, and prognosis of GEP-NENs. Through an extensive literature search encompassing studies up to April 2024, we examined various factors, including obesity, malnutrition, metabolic syndrome and type 2 diabetes mellitus, and their roles in the development and progression of GEP-NENs.
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Hôpital Edouard Herriot, Lyon, France.
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December 2024
Department of Medicinal Chemistry, Uppsala University, BMC P.O. Box 574, SE-751 23, Uppsala, Sweden. Electronic address:
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