Rapid and extensive hepatic destruction (e.g., severe toxic hepatitis) causes fasting hypoglycemia because the liver is the major site of endogenous glucose production. The mechanism of hypoglycemia reported in patients with cardiac failure is unknown but likely involves hepatic congestion. Although the kidneys are a source of glucose production, it is perhaps too simplistic to attribute hypoglycemia in persons with renal failure to this mechanism alone. The clearance of insulin is reduced substantially in renal failure, and reduced mobilization of gluconeogenic precursors has been reported.
Sepsis is sometimes complicated by hypoglycemia, which is multifactorial in origin. There is impaired endogenous glucose production, perhaps a result of hepatic hypoperfusion, and increased glucose utilization, which is induced by cytokines in macrophage-rich tissues such as the liver, spleen, and ileum and in muscle. Nutrition is also often inadequate in the setting of sepsis. Hypoglycemia can be seen with prolonged starvation, perhaps because of a loss of whole-body fat stores and the subsequent depletion of gluconeogenic precursors (e.g., amino acids), which necessitate increased glucose utilization.
제 생각에는 insulin에 대한 renal clearance가 감소한 경우라면 plasma insulin level이 증가하겠지만, 증가한다는 말에 대한 뚜렷한 업급이 책에 잘 보이지 않네요.
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항상 말하듯이 본인은 답변의 정확성 및 내용에 대한 아무런 책임을 지지 않으며, 참고사항으로 답변을 제공합니다.
Critical Illness
Rapid and extensive hepatic destruction (e.g., severe toxic hepatitis) causes fasting hypoglycemia because the liver is the major site of endogenous glucose production. The mechanism of hypoglycemia reported in patients with cardiac failure is unknown but likely involves hepatic congestion. Although the kidneys are a source of glucose production, it is perhaps too simplistic to attribute hypoglycemia in persons with renal failure to this mechanism alone. The clearance of insulin is reduced substantially in renal failure, and reduced mobilization of gluconeogenic precursors has been reported.
Sepsis is sometimes complicated by hypoglycemia, which is multifactorial in origin. There is impaired endogenous glucose production, perhaps a result of hepatic hypoperfusion, and increased glucose utilization, which is induced by cytokines in macrophage-rich tissues such as the liver, spleen, and ileum and in muscle. Nutrition is also often inadequate in the setting of sepsis. Hypoglycemia can be seen with prolonged starvation, perhaps because of a loss of whole-body fat stores and the subsequent depletion of gluconeogenic precursors (e.g., amino acids), which necessitate increased glucose utilization.
제 생각에는 insulin에 대한 renal clearance가 감소한 경우라면 plasma insulin level이 증가하겠지만, 증가한다는 말에 대한 뚜렷한 업급이 책에 잘 보이지 않네요.
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항상 말하듯이 본인은 답변의 정확성 및 내용에 대한 아무런 책임을 지지 않으며, 참고사항으로 답변을 제공합니다.