在肥胖的年轻人中,因克雷丁效应决定了葡萄糖轨迹和胰岛素敏感性
Alfonso Galderisi1, Domenico Tricò2, Jessica Lat1
1Yale University, Department of Pediatrics, New Haven, Connecticut, USA.
JCI insight
|October 17, 2023
概括
在肥胖的年轻人中,在青春期更强的隐素效应可以改善β细胞功能和长期胰岛素敏感性. 减弱的英克雷丁效应预示着较差的葡萄糖控制和体重轨迹.
科学领域:
- 代谢和内分泌学
- 儿童肥胖研究儿童肥胖研究
- 糖尿病病理生理学 糖尿病病理生理学
背景情况:
- 胰岛素分泌的肠道激素强化,因克列效应,在肥胖的年轻人中减弱.
- 了解在青春期过渡期间因克雷丁效应的纵向影响对于管理肥胖青少年的代谢健康至关重要.
研究的目的:
- 研究因克雷丁对β细胞功能和肥胖青少年胰岛素敏感性的长期影响.
- 为了确定基线英克雷丁效应是否会影响青春期过渡期间的葡萄糖代谢和体重的轨迹.
主要方法:
- 一组患有葡萄糖耐受性损害的肥胖年轻人接受了口服葡萄糖耐受性测试 (OGTT) 和同糖血症静脉输血葡萄糖,以量化因克雷丁的效果.
- 参与者在2年后被重新评估,随访数据按基线的分层分层.
主要成果:
- 在随访时,高基线的胰岛素效应与改善的β细胞功能 (DIMM) 和增强的胰岛素敏感性有关.
- 较低的基线因克雷丁效应预测了随访时更高的1和2小时葡萄糖水平.
- 虽然GLP-1水平最初有所不同,但在随访时,在低缩蛋白组中,葡萄糖抑制显著降低.
结论:
- 青春期过渡期间的素效应显著影响了肥胖年轻人的β细胞功能和体重管理的纵向过程.
- 保持或增强因克列效应可能是改善这种人群代谢结果的关键治疗目标.
相关概念视频
Glucagon-like Receptor Agonists
334
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...
334
Glucose Homeostasis: Pancreatic Islets and Insulin Secretion
1.3K
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...
1.3K
Insulin: Dosing Regimen and Adverse Effects
184
Insulin-replacement therapy usually includes both long-acting insulin (basal) and short-acting insulin (to cater to postprandial needs). In a diverse group of type 1 diabetes patients, the average daily insulin dose is typically 0.5-0.7 units/kg body weight. However, obese patients and pubertal adolescents may need more due to insulin resistance.
The basal dose constitutes about 40%-50% of the total daily dose, with the rest as premeal insulin. The mealtime insulin dose should mirror...
The basal dose constitutes about 40%-50% of the total daily dose, with the rest as premeal insulin. The mealtime insulin dose should mirror...
184
Hormones Regulating Blood Glucose
3.4K
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...
3.4K
Oral Hypoglycemic Agents: Biguanides and Glitazones
212
Biguanides, particularly metformin (Glucophage), are insulin sensitizers that enhance glucose uptake, thereby reducing insulin resistance. Unlike sulfonylureas, metformin doesn't prompt insulin secretion, which helps to curb hypoglycemia risk. Metformin is beneficial in treating conditions like polycystic ovary syndrome due to its insulin-resistance reduction capability. The drug's primary action involves curtailing hepatic gluconeogenesis, a significant contributor to high blood...
212
Hypoglycemia and Glucagon
274
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...
274


