β-基酸盐促进基底胰岛素分泌,同时降低小鼠和人类小岛的葡萄糖分泌
Risha Banerjee1, Ying Zhu1, George P Brownrigg1
1Department of Cellular and Physiological Sciences, Life Sciences Institute, University of British Columbia, Vancouver, BC V6T 2A1, Canada.
Endocrinology
|July 6, 2024
概括
在低碳水化合物饮食中产生的酸乙酸 (βHB),增强胰岛素分泌,减少胰腺小岛的葡萄糖分泌. 这一发现表明βHB在调节小岛细胞功能和激素信号传递方面发挥作用.
科学领域:
- 内分泌学 在内分泌学.
- 代谢科学 代谢科学
- 分子生物学分子生物学
背景情况:
- 饮食中的碳水化合物会影响血糖和2型糖尿病的管理.
- 低碳水化合物摄入量有助于脂肪的利用和的产生,包括β-基酸盐 (βHB).
- βHB对胰腺小岛细胞功能的直接影响尚不清楚.
研究的目的:
- 为了研究β-hydroxybutyrate (βHB) 对人类小岛细胞分泌反应的影响.
- 确定R-βHB和S-βHB反体对胰岛素和葡萄糖分泌的特定作用.
- 探索βHB对小岛细胞的影响背后的分子机制.
主要方法:
- 人类和小鼠小岛的急性治疗是用赛血型βHB和单个反体 (R-βHB,S-βHB).
- 在不同的葡萄糖度下测量胰岛素和葡萄糖分.
- 在72小时内用R-βHB治疗的人类小岛的蛋白质组分析.
主要成果:
- 急性βHB治疗在人类小岛中增加了低葡萄糖 (3mM) 的胰岛素分泌.
- 在人体和小鼠小岛上,R-βHB反体在生理葡萄糖水平上特别增加了胰岛素分泌和降低了葡萄糖分泌.
- 蛋白质组分析显示R-βHB治疗小岛的蛋白质丰度发生变化,可能促进细胞健康和存活.
结论:
- 生物学的βHB度,特别是R-βHB,直接影响胰腺小岛的激素分泌.
- βHB影响胰岛素和葡萄糖释放,这表明它在葡萄糖平衡中起着调节作用.
- R-βHB可能有助于小岛细胞的健康和生存,这需要进一步研究糖尿病治疗潜力.
相关概念视频
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion
1.2K
The pancreatic islets comprising only 1%-2% of the volume are highly vascularized and innervated mini-organs. They contain five endocrine cell types, including β cells that secrete insulin, which is synthesized as a single polypeptide chain, preproinsulin, processed to proinsulin, and finally to insulin and C-peptide. This process is complex and regulated, involving the Golgi complex, the endoplasmic reticulum, and the secretory granules of the β cell.
Insulin and C-peptide are...
Insulin and C-peptide are...
1.2K
Hormones Regulating Blood Glucose
3.2K
Insulin is released by beta cells of the pancreas when blood glucose levels are high. It facilitates glucose absorption and utilization in insulin-dependent cells with insulin receptors on their plasma membranes. Insulin promotes glucose uptake by increasing the number of glucose transport proteins in the cell membrane, allowing glucose to enter the cell. As a result, glucose utilization and ATP production are enhanced.
In addition to accelerating glucose uptake and utilization, insulin has...
In addition to accelerating glucose uptake and utilization, insulin has...
3.2K
Insulin Secretory Vesicles
4.9K
Insulin secretory vesicles release insulin to stimulate blood glucose uptake and regulate carbohydrate metabolism. When the blood glucose levels increase, glucose enters the pancreatic β-islet cells through glucose transporters. Once inside, glucose is metabolized through glycolysis, the citric acid cycle, and the electron transport chain, producing ATP. This increase in ATP concentration closes ATP-sensitive potassium channels, leading to depolarization of the membrane and the opening of...
4.9K
Insulin: Biosynthesis, Chemistry, and Preparation
370
The endoplasmic reticulum (ER) of pancreatic β-cells synthesizes preproinsulin, which consists of a signal peptide, A and B chains, and a C-peptide. Preproinsulin is then cleaved and folded into proinsulin, which translocates to the Golgi apparatus for sorting and packaging into secretory granules. In these granules, enzymatic clipping generates insulin and C-peptide.
Damage or functional impairment of β-cells inhibits insulin production, leading to diabetes. Diabetes treatment...
Damage or functional impairment of β-cells inhibits insulin production, leading to diabetes. Diabetes treatment...
370
Glucagon-like Receptor Agonists
313
Incretins include glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), which stimulate insulin secretion post-meals. In type 2 diabetes, GIP's efficacy is reduced, making GLP-1 a viable drug target. GIP originates from preproGIP.
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
GLP-1, when administered in high doses intravenously, triggers insulin secretion, inhibits glucagon release, slows gastric emptying, reduces food intake, and restores normal insulin secretion. However, its rapid inactivation by...
313
Hypoglycemia and Glucagon
254
Without prolonged fasting, healthy individuals maintain blood glucose levels above 3.5 mM due to a well-adapted neuroendocrine counterregulatory system that effectively prevents acute hypoglycemia, a potentially life-threatening condition. The primary clinical scenarios for hypoglycemia encompass diabetes treatment, inappropriate production of endogenous insulin or insulin-like substances by tumors, and the use of glucose-lowering agents in non-diabetic individuals. Notably, hypoglycemia in the...
254


