Human growth hormone (GH) is a peptide hormone synthesized, stored, and secreted by the somatotropic cells within the anterior pituitary gland. While known for stimulating growth in children, its role in adults shifts to maintaining body structure and regulating fundamental metabolic processes. Metabolism is the process of converting food into the energy needed to sustain life. GH exerts a profound influence on this energy balance, coordinating the utilization of fats, carbohydrates, and proteins to meet the body’s demands.
Shifting Energy Sources: The Effect on Fat Metabolism
Growth hormone acts as a catabolic agent on fat tissue, promoting the breakdown and mobilization of stored energy reserves. This process, known as lipolysis, converts triglycerides stored in fat cells into free fatty acids (FFAs) and glycerol. The FFAs are released into the bloodstream, where they become the preferred fuel source for many tissues, such as muscle.
This metabolic shift is evident during periods of fasting or high energy demand, where GH secretion increases to ensure energy availability. By encouraging the burning of fat for fuel, GH conserves the body’s stores of glucose and protein, a process known as protein sparing. The released glycerol travels to the liver, where it can be used for the creation of new glucose.
Regulating Blood Sugar: The Effect on Glucose Handling
GH has a counter-regulatory or anti-insulin effect on carbohydrate metabolism. This means GH actively works to raise blood sugar levels, leading to its description as a diabetogenic hormone. GH achieves this by inducing insulin resistance in peripheral tissues, primarily skeletal muscle and fat cells.
The presence of GH makes these cells less responsive to insulin, hindering the uptake of glucose from the bloodstream. Simultaneously, GH stimulates the liver to increase glucose output through glycogenolysis (breakdown of stored glycogen) and gluconeogenesis (creation of new glucose from non-carbohydrate sources). Higher levels of circulating FFAs from GH-induced lipolysis also interfere with insulin signaling, exacerbating insulin resistance. This coordinated effort ensures that glucose remains available in the circulation, primarily for tissues like the brain.
Promoting Growth: The Effect on Protein Synthesis
The anabolic effects of GH are primarily mediated through its stimulation of protein synthesis, which is fundamental for tissue growth and repair. GH achieves this by stimulating the liver to produce Insulin-like Growth Factor 1 (IGF-1), a hormone structurally similar to insulin. Both GH and IGF-1 work synergistically to increase the uptake of amino acids by cells and accelerate the rate at which new proteins are built.
This dual action also suppresses the breakdown of existing proteins (catabolism), leading to a state of positive nitrogen balance. This means the body retains more nitrogen—a core component of amino acids—than it excretes, which is necessary for muscle development and the growth of most body organs. While GH directly influences fat and glucose metabolism acutely, the protein-building effects, largely driven by IGF-1, represent a sustained and long-term metabolic outcome.
Metabolic Consequences of GH Imbalances
Chronic disruption of normal GH levels leads to significant metabolic dysfunction. When GH levels are chronically too low, Growth Hormone Deficiency (GHD) results in a distinct metabolic profile in adults. These patients often exhibit a higher amount of visceral fat and a reduction in lean muscle mass.
This GH-deficient state is associated with unfavorable changes in blood lipids, such as elevated triglycerides and lower levels of high-density lipoprotein (HDL) cholesterol. Paradoxically, though the body becomes more sensitive to insulin, the altered body composition—particularly the excess visceral fat—can still lead to overall insulin resistance and a higher cardiovascular risk over time.
The metabolic picture is dramatically different with chronic GH excess, such as in acromegaly, a condition usually caused by a pituitary tumor. The prolonged high levels of GH in acromegaly lead to severe insulin resistance and impaired glucose tolerance, which frequently progresses to overt type 2 diabetes. The mechanisms that raise blood sugar are exaggerated, causing chronic hyperglycemia that overwhelms the body’s compensatory mechanisms. Furthermore, the excessive tissue growth characteristic of acromegaly, combined with the metabolic stress, contributes to enlarged organs and increased risk of heart disease. These pathological states demonstrate that long-term metabolic health depends on the coordinated balance of GH’s effects on all three macronutrient pathways.