由于酸氨基醇-3激酶 (PI3K) 抑制而导致的二次高血糖症
Arunan Sriravindrarajah1,2, Joshua Hurwitz1,2,3,4, Elgene Lim1,2,3,4
1St Vincent's Hospital, Sydney, Australia.
Endocrinology, diabetes & metabolism case reports
|October 22, 2024
概括
像Inavolisib这样的新型PI3K抑制剂可以在癌症患者中引起高血糖症. 最小化高胰岛素血症的策略是首选的,以保持这些PI3K抑制剂的抗癌有效性.
科学领域:
- 在瘤学瘤学.
- 药理学 药理学是指药理学的学科.
- 内分泌学 在内分泌学.
背景情况:
- 酸丁醇-3激酶 (PI3K) 途径对细胞生长,新陈代谢和生存至关重要,并与许多人类癌症有关.
- PI3K抑制剂已被批准用于乳腺癌和淋巴瘤,其他癌症正在进行试验.
- PI3K调解胰岛素作用,其抑制可以导致高血糖症,这是一个显著的副作用.
研究的目的:
- 报告患有转移性乳腺癌患者急性3级高血糖症的病例,该患者接受了新型PI3K抑制剂inavolisib.
- 审查PI3K抑制剂相关高血糖症的治疗选择.
- 讨论高胰岛素血症对PI3K抑制剂疗效的影响.
主要方法:
- 一个53岁的女性患有转移性乳腺癌的病例报告.
- 对PI3K抑制剂诱导的高血糖症治疗策略的审查.
- 关于高胰岛素血症和PI3K通路再激活的动物模型数据的分析.
主要成果:
- 患者因因沃利西布治疗而发展出急性3级高血糖症.
- 胰岛素高血压可能通过部分重新激活该途径来抵消PI3K抑制剂的抗癌作用.
- 建议采用替代的高血糖管理策略,尽量减少高胰岛素血症.
结论:
- 虽然PI3K抑制剂是有效的癌症治疗药物,但它们存在高血糖症的风险.
- 高血糖的管理应考虑对PI3K抑制剂疗效的潜在影响.
- 通过低碳水化合物饮食或甲福明等替代治疗来最大限度地减少高胰岛素血症可能对持续的抗癌活性至关重要.
更多相关视频
06:51Utilizing 18F-FDG PET/CT Imaging and Quantitative Histology to Measure Dynamic Changes in the Glucose Metabolism in Mouse Models of Lung Cancer
Published on: July 21, 2018
17.9K
11:06Human Liver Microphysiological System for Assessing Drug-Induced Liver Toxicity In Vitro
Published on: January 31, 2022
4.3K
相关概念视频
Dipeptidyl Peptidase 4 Inhibitors
173
Dipeptidyl peptidase 4 (DPP-4) is a serine protease widely distributed in the body. It's involved in the inactivation of GLP-1 and GIP hormones, which are crucial for insulin regulation. DPP-4 inhibitors, such as sitagliptin (Januvia), saxagliptin (Onglyza), linagliptin (Tradjenta), alogliptin (Nesina), and vildagliptin (Galvus), help increase the proportion of active GLP-1, enhancing insulin secretion. These inhibitors work by competitively binding to DPP-4. This binding causes a...
173
PI3K/mTOR/AKT Signaling Pathway
3.4K
The mammalian target of rapamycin (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1 (mTORC1) and mTOR complex 2 (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast, mTORC2 consists of a...
3.4K
Oral Hypoglycemic Agents: Biguanides and Glitazones
176
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...
176
Hypoglycemia and Glucagon
153
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...
153
Oral Hypoglycemic Agents: Glinides
142
Repaglinide (Prandin) and Nateglinide (Starlix), known as glinides, are oral insulin secretagogues that stimulate insulin release from pancreatic β cells by closing the ATP-sensitive potassium channels (KATP channel). Repaglinide controls insulin release from pancreatic β cells by managing potassium efflux. It shares two binding sites with sulfonylureas and also has a unique site, indicating overlapping mechanisms of action. With a rapid onset and a 4-7 hour duration, it effectively...
142
Phosphoinositides and PIPs
8.5K
Phosphoinositides are a group of phospholipids containing a glycerol backbone with two fatty acid chains and a phosphate attached to a myoinositol sugar ring. The inositol head group extends into the cytoplasm, where it is modified by adding phosphate groups to form phosphatidylinositol phosphates or PIPs.
Different phosphoinositides are synthesized and recruited on the cytosolic face of the plasma membrane. The localization of specific phosphoinositides concentrated in separate membrane...
Different phosphoinositides are synthesized and recruited on the cytosolic face of the plasma membrane. The localization of specific phosphoinositides concentrated in separate membrane...
8.5K
