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What is the Relationship Between Growth Hormone and Glucose?

Published in Glucose-GH Interaction 2 mins read

Growth hormone (GH) has a complex relationship with glucose, impacting blood sugar levels both directly and indirectly. Essentially, GH raises blood glucose levels.

Direct Effects of GH on Glucose

GH directly affects glucose metabolism through several mechanisms:

  • Increased Glucose Production: GH stimulates the liver to produce more glucose through gluconeogenesis (creation of glucose from non-carbohydrate sources) and glycogenolysis (breakdown of glycogen, stored glucose). This increases blood glucose levels.
  • Reduced Glucose Uptake: GH promotes insulin resistance, meaning the body's cells become less responsive to insulin. Insulin is crucial for glucose uptake from the bloodstream into cells. Decreased insulin sensitivity leads to higher blood glucose levels.
  • Increased Lipolysis: GH stimulates the breakdown of fats (lipolysis), providing alternative energy sources and reducing the body's reliance on glucose. While this might seem counterintuitive, it also contributes to higher blood sugar.

Indirect Effects of GH on Glucose

GH's indirect effects on glucose involve its interaction with Insulin-like Growth Factor 1 (IGF-I):

  • IGF-I and Glucose: GH stimulates the production of IGF-I, which also plays a role in glucose metabolism. The exact nature of IGF-I's influence on glucose is complex and can vary depending on several factors, but it generally interacts with the direct effects of GH.

In summary: GH's primary action is to increase blood glucose levels. It does this by boosting glucose production in the liver and reducing the effectiveness of insulin in lowering blood sugar. Its indirect effects through IGF-I further contribute to this overall impact. The reference explicitly states: "GH regulates glucose homeostasis directly, by inducing glycogenolysis, gluconeogenesis, and lipolysis and promoting insulin resistance, and indirectly, via IGF-I production. Primarily, GH inhibits insulin-induced suppression of hepatic gluconeogenesis, thus increasing glucose production."

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