Somatostatin is an endogenous inhibitor of secretion and cell proliferation. These features render somatostatin a logical candidate for the management of neuroendocrine tumors that express somatostatin receptors. Synthetic somatostatin analogs (SSAs) have longer half-lives than somatostatin, but have similar activities, and are used for the treatment of these types of disorders. Interest has focused on novel multireceptor analogs with broader affinity to several of the five somatostatin receptors, thereby presenting putatively higher antitumor activities. Recent evidence indicates that SSAs cannot be considered mimics of native somatostatin in regulating signaling pathways downstream of receptors. Here we review this knowledge, discuss the concept of biased agonism, and highlight what considerations need to be taken into account for the optimal clinical use of SSAs.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.tem.2013.11.003 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Detection of Insulin in Insulin-Deficient Islets of Patients with Type 1 Diabetes.
Life (Basel)
January 2025
Laboratory of Nervous System Development, Avtsyn Research Institute of Human Morphology of Federal State Budgetary Scientific Institution "Petrovsky National Research Centre of Surgery", Tsurupi Street, 3, 117418 Moscow, Russia.
Type 1 diabetes (T1D) is related to the autoimmune destruction of β-cells, leading to their almost complete absence in patients with longstanding T1D. However, endogenous insulin secretion persists in such patients as evidenced by the measurement of plasma C-peptide. Recently, a low level of insulin has been found in non-β islet cells of patients with longstanding T1D, indicating that other islet cell types may contribute to persistent insulin secretion.
View Article and Find Full Text PDFDifferential Impact of Medical Therapies for Acromegaly on Glucose Metabolism.
Int J Mol Sci
January 2025
Endocrinology Unit, Department of Internal Medicine and Medical Specialties, School of Medical and Pharmaceutical Sciences, University of Genova, 16132 Genova, Italy.
Acromegaly is a rare endocrine disorder caused by excessive growth hormone (GH) production, due, in the vast majority of cases, to the presence of a GH-secreting pituitary tumour. The chronic elevation of GH and the resulting high circulating levels of insulin-like growth factor-1 (IGF-1) cause the characteristic tissue overgrowth and a number of associated comorbidities, including several metabolic changes, such as glucose intolerance and overt diabetes mellitus (DM). Elevated GH concentrations directly attenuate insulin signalling and stimulate lipolysis, decreasing glucose uptake in peripheral tissues, thus leading to the development of impaired glucose tolerance and DM.
View Article and Find Full Text PDFSSTR2-Targeted Theranostics in Hepatocellular Carcinoma.
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.
Small Bowel Leiomyoma Mimics Neuroendocrine Tumor on 68Ga-DOTATATE PET/CT.
Clin Nucl Med
January 2025
Department of Nuclear Medicine, Royal Free London NHS Foundation Trust, London, United Kingdom.
A 57-year-old man with a 3-month history of lower abdominal pain and rectal bleeding with black stools underwent urgent abdominal CT, which revealed an ovoid hyperdense lesion in the ileum in the right iliac fossa. The prime differential was a midgut neuroendocrine tumor. Thus, the patient was referred for a 68Ga-DOTATATE PET/CT scan, which demonstrated intense activity in this lesion with no evidence of somatostatin receptor expression elsewhere.
View Article and Find Full Text PDFAlterations in Prefrontal Cortical Somatostatin Neurons in Schizophrenia: Evidence for Weaker Inhibition of Pyramidal Neuron Dendrites.
Biol Psychiatry
January 2025
Translational Neuroscience Program, Department of Psychiatry, School of Medicine, University of Pittsburgh; Department of Neuroscience, Dietrich School of Arts and Sciences, University of Pittsburgh; Center for the Neural Basis of Cognition, Carnegie Mellon University. Electronic address:
Background: Certain cognitive processes require inhibition provided by the somatostatin (SST) class of gamma-aminobutyric acid (GABA) neurons in the dorsolateral prefrontal cortex (DLPFC). This inhibition onto pyramidal neuron dendrites depends on both SST and GABA signaling. Although SST mRNA levels are lower in the DLPFC in schizophrenia, it is not known if SST neurons exhibit alterations in the capacity to synthesize GABA, principally via the 67-kilodalton isoform of glutamic acid decarboxylase (GAD67).
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!