1. The effect of the long-acting somatostatin analogue SMS-201995 on diabetes control was assessed in 6 insulin-dependent diabetic patients (3 men and 3 women aged 19-38 years). 2. Plasma glucose and triglyceride profiles were obtained on 4 consecutive days, from 8:00 a.m. to 2:00 p.m. On the first 2 days the patients received their usual dose of insulin and ate at 8:00 a.m. and at noon. On the third and fourth days they received 1/3 of their usual insulin dose together with 100 micrograms SMS-201995 injected subcutaneously. 3. Postprandial glucose and triglyceride increases were blunted during the 360 min of observation on both days after SMS-201995 administration. The areas under the glucose-time plots fell from 23.72 +/- 12.29 (mean +/- SD) to 7.98 +/- 14.26 (P < 0.05) and the areas under the triglyceride-time plots from 10.51 +/- 9.01 to -3.15 +/- 4.30 g.min.dl-1 (P < 0.01). 4. No adverse reactions were observed after SMS-201995 administration for 2 days. 5. We conclude that administration of the somatostatin analogue SMS-201995 may be beneficial for insulin-dependent diabetic patients.
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Cancers (Basel)
January 2025
The Brown Foundation Institute of Molecular Medicine, McGovern Medical School, The University of Texas Health Science Center, Houston, TX 77054, USA.
Background: While the clinical use of radiolabeled somatostatin analogs is well established in neuroendocrine tumors, there is growing interest in expanding their application to other somatostatin receptor 2 (SSTR2)-expressing cancers. This study investigates the potential utility of SSTR2-targeted theranostics in hepatocellular carcinoma (HCC).
Methods: SSTR2 expression in HCC cell lines and clinical samples was evaluated using qRT-PCR, Western blot analysis, and a public dataset.
Front Oncol
January 2025
Department of Nuclear Medicine, Mount Sinai Hospital at Icahn School of Medicine, New York, NY, United States.
Peptide receptor radionuclide therapy (PRRT) is used for the management of neuroendocrine tumors (NETs) not responsive to somatostatin analogs. In this case series, we report two patients with pancreatic vasoactive intestinal peptide (VIP)-secreting NETs (VIPomas) not responsive to any other therapies who achieved symptomatic control and a significant decrease in serum VIP levels with PRRT during their hospital stay. Two patients with VIPomas were admitted to the hospital with multiple prior hospital admissions after going through multiple lines of therapy.
View Article and Find Full Text PDFCurr Treat Options Oncol
January 2025
The Sidney Kimmel Comprehensive Cancer Center at Johns Hopkins and Department of Oncology, Johns Hopkins University School of Medicine, Baltimore, MD, 21287, USA.
Treatment for neuroendocrine neoplasms (NENs) is tailored to the tumor's site of origin, grade, and differentiation. NENs are categorized into two main types: well-differentiated neuroendocrine tumors (NETs), which tend to grow more slowly and are less aggressive, and poorly differentiated neuroendocrine carcinomas (NECs), which are highly aggressive and harder to treat. Treatment options for NETs range from somatostatin analogues and mTOR inhibitors to peptide receptor radionuclide therapy (PRRT) with Lutetium-177 dotatate.
View Article and Find Full Text PDFEndocr J
January 2025
Department of Molecular Diagnosis, Chiba University Graduate school of Medicine, Chiba 260-8670, Japan.
Pasireotide (PAS), a multireceptor somatostatin analog, has been demonstrated to effectively control hormone levels, including those of growth hormone (GH) and insulin-like growth factor 1 (IGF-1), in patients with acromegaly. However, it induces hyperglycemia by inhibiting insulin secretion via somatostatin receptor 5 (SSTR5). Despite the extensive literature on the occurrence of PAS-induced hyperglycemia, there is still no consensus on the optimal first-line treatment for this complication.
View Article and Find Full Text PDFRev Endocr Metab Disord
January 2025
Department of Medicine, Division of Endocrinology, Diabetes, and Metabolism, University of Illinois at Chicago, Chicago, IL, USA.
This review focuses on our current understanding of how growth hormone releasing hormone (GHRH): 1) stimulates GH release and synthesis from pituitary growth hormone (GH)-producing cells (somatotropes), 2) drives somatotrope proliferation, 3) is negatively regulated by somatostatin (SST), GH and IGF1, 4) is altered throughout lifespan and in response to metabolic challenges, and 5) analogues can be used clinically to treat conditions of GH excess or deficiency. Although a large body of early work provides an underpinning for our current understanding of GHRH, this review specifically highlights more recent work that was made possible by state-of-the-art analytical tools, receptor-specific agonists and antagonists, high-resolution in vivo and ex vivo imaging and the development of tissue (cell) -specific ablation mouse models, to paint a more detailed picture of the regulation and actions of GHRH.
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