Interactions between endocrine α and β cells are critical to their secretory function in vivo. The interactions are highly regulated, although yet to be fully understood. In this study, we aim to assess the impact of α and β cell co-culture on hormone secretion. Mouse clonal cell lines α-TC6-1 (α cell line) and MIN-6 (β cell line) were cultured independently or in combination in a medium containing 5.5, 11.1, or 25 mM glucose, respectively. After 72 h, hormone release was measured using insulin and glucagon secretion assays, the cell distribution was visualized by inverted microscopy and an immunocytochemistry assay, and changes in gene expressions were assessed using the RT-PCR technique. The co-culture of the two cell lines caused a decrease in glucagon secretion from α-TC1-6 cells, while no effect on insulin secretion from MIN-6 cells was revealed. Both types of cells were randomly scattered throughout the culture flask, unlike in mice islets in vivo where β cells cluster in the core and α cells are localized at the periphery. During the α-β cell co-culture, the gene expression of glucagon (Gcg) decreased significantly. We conclude that islet β cells suppress glucagon secretion from α cells, apparently via direct cell-to-cell contact, of which the molecular mechanism needs further verification.

Download full-text PDF

Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8308288PMC
http://dx.doi.org/10.3390/nu13072281DOI Listing

Publication Analysis

Top Keywords

glucagon secretion
16
cells
9
secretion cells
8
cell
8
α-β cell
8
cell co-culture
8
cell lines
8
secretion
6
glucagon
5
pancreatic cells
4

Similar Publications

Type 2 Diabetes Mellitus Exacerbates Pathological Processes of Parkinson's Disease: Insights from Signaling Pathways Mediated by Insulin Receptors.

Neurosci Bull

January 2025

Center for Translational Neuromedicine and Neurology, School of Life Sciences, Institute for Brain Sciences Research, Henan University, Huaihe Hospital of Henan University, Kaifeng, 475004, China.

Parkinson's disease (PD), a chronic and common neurodegenerative disease, is characterized by the progressive loss of dopaminergic neurons in the dense part of the substantia nigra and abnormal aggregation of alpha-synuclein. Type 2 diabetes mellitus (T2DM) is a metabolic disease characterized by chronic insulin resistance and deficiency in insulin secretion. Extensive evidence has confirmed shared pathogenic mechanisms underlying PD and T2DM, such as oxidative stress caused by insulin resistance, mitochondrial dysfunction, inflammation, and disorders of energy metabolism.

View Article and Find Full Text PDF

The effect of long-chain n-3 PUFA on liver transcriptome in human obesity.

Prostaglandins Leukot Essent Fatty Acids

December 2024

Department of Medicine III, Division of Endocrinology and Metabolism, Medical University of Vienna, Austria; Department of Medicine III and Karl Landsteiner Institute for Metabolic Diseases and Nephrology, Clinic Hietzing, Vienna, Austria. Electronic address:

Background And Aims: Obesity is associated with a higher risk of severe diseases such as atherosclerotic cardiovascular disease, type 2 diabetes mellitus (T2DM), and metabolic dysfunction-associated steatotic liver disease (MASLD). Polyunsaturated fatty acids, of the omega-3 family (n-3 PUFA), have been shown to reduce adipose tissue inflammation in obesity, as well as to have lipid-lowering effects and improve insulin sensitivity. However, direct effects on liver transcriptome in humans have not been described.

View Article and Find Full Text PDF

Tirzepatide is a dual agonist of glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) receptors and is a promising therapeutic option for type 2 diabetes mellitus (T2DM). Nevertheless, its effect and underlying mechanism on hepatic steatosis remain ambiguous. Herein, we explored the impact of tirzepatide on improving hepatic steatosis in diabetic mice, with a particular focus on the gut microbiota and bile acids (BAs) using animal models.

View Article and Find Full Text PDF

Neuroendocrine tumors and diabetes mellitus: which treatment and which effect.

Endocrine

January 2025

Unit of Endocrinology, Department of Clinical and Molecular Medicine, ENETS Center of Excellence, Sapienza University of Rome, Rome, Italy.

Diabetes mellitus (DM) and neuroendocrine tumors (NET) can exert unfavorable effects on each other prognosis. In this narrative review, we evaluated the effects of NET therapies on glycemic control and DM management and the effects of anti-diabetic therapies on NET outcome and management. For this purpose, we searched the PubMed, Science Direct, and Google Scholar databases for studies reporting the effects of NET therapy on DM as well as the effect of DM therapy on NET.

View Article and Find Full Text PDF

Background: High age is the biggest risk factor for Alzheimer's disease (AD). Approved drugs that slow down the aging process have the potential to be repurposed for the primary prevention of AD. The aim of our project was to use a reverse translational approach to identify such drug candidates in epidemiological data followed by validation in cell-based models and animal models of aging and AD.

View Article and Find Full Text PDF

Want 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!