GH antagonizes the action of insulin in skeletal muscle and adipose tissue at the postreceptor level. However, it does not have the same effect on the liver. The removal of the pituitary gland (hypophysectomy) can actually improve diabetic management because both GH and cortisol decrease insulin sensitivity. Due to its ability to cause insulin insensitivity, GH is considered a diabetogenic hormone. Therefore, excessive secretion of GH, such as in acromegaly, can lead to diabetes mellitus and an increased need for insulin to maintain normal metabolism. Furthermore, excess insulin secretion resulting from an excess of GH can cause damage to pancreatic beta cells. In the absence of GH, insulin secretion decreases. This highlights the importance of normal GH levels for pancreatic function and insulin secretion.

While GH deficiency in adults is recognized as a pathological syndrome, it does not impair growth if it occurs after the closure of the epiphyses. GH deficiency is one of the potential causes of hypoglycemia. Recent studies have shown that prolonged deficiencies of GH can lead to changes in body composition, with an increase in body fat percentage and a decline in lean body mass. Muscle weakness and early exhaustion are also symptoms of GH deficiency. There has been interest in using GH in elderly populations to reverse age-related physical decline and changes in body composition, but studies have only shown minimal changes in body composition, no functional benefits, and an increased risk of adverse events.

GH is necessary for growth before adulthood. Deficiencies in GH result in severe growth deficits, while excess GH causes gigantism. In adulthood, excess GH after epiphyseal closure leads to acromegaly, characterized by the gradual enlargement of the hands and feet, coarsening of facial features, insulin resistance, and diabetes. Genetic disorders affecting the GH-IGF-I axis can cause significant growth impairments. Mutations in the GH and GHRH receptor genes are the most common causes of isolated GH deficiency. Patients with these mutations can be treated with recombinant GH to restore the function of the downstream axis. In Laron syndrome, a mutation of the GH receptor results in GH resistance. In this case, the liver fails to produce IGF-I due to a lack of responsiveness to GH. These patients can be treated with IGF-I, but the effectiveness of the treatment is limited without the direct actions of GH. Other downstream genetic mutations that have been reported include those in STAT5B, IGF-I, and ALS.

The lactotrope is responsible for producing prolactin, a single-chain protein consisting of 199 amino acids. Prolactin, like GH and hPL, belongs to the cytokine family and is coupled to the JAK/STAT signaling pathways through the PRL receptor. In humans, the primary role of prolactin is related to breast development and function during pregnancy and lactation. Therefore, the regulation and actions of prolactin will be discussed in detail in relation to these processes.

It is important to note that the lactotrope differs from the other endocrine cell types in the adenohypophysis in two major ways. Firstly, it is not part of an endocrine axis. This means that PRL acts directly on nonendocrine cells, primarily in the breast, to induce physiological changes. Secondly, the lactotrope produces prolactin, which has distinct functions compared to the hormones produced by other endocrine cells in the pituitary gland.
GH antagonizes the action of insulin at the postreceptor level in skeletal muscle and adipose tissue (but not the liver). Hypophysectomy (removal of the pituitary gland) can improve diabetic management because GH, like cortisol, decreases insulin sensitivity. Because GH produces insulin insensitivity, it is considered a diabetogenic hormone. Therefore when secreted in excess (e.g., in acromegaly), GH can cause diabetes mellitus, and the insulin levels necessary to maintain normal metabolism increase. Excessive insulin secretion resulting from an excess of GH can cause damage to pancreatic beta cells. In the absence of GH, insulin secretion declines. Thus normal levels of GH are required for normal pancreatic function and insulin secretion.
GH deficiency in adults is becoming recognized as a pathological syndrome. If GH deficiency occurs after the epiphyses close, growth is not impaired. GH deficiency is one of many possible causes of hypoglycemia. Recent studies have shown that extended deficiencies of GH lead to changes in body composition. Fat as a percentage of body weight increases, whereas lean body mass declines. In addition, muscle weakness and early exhaustion are symptoms of GH deficiency. There has been interest in using GH in elderly populations to reverse age-related physical decline and body composition, but studies to date have shown small changes in body composition, no functional benefits, and increased risk of adverse events.
GHisnecessaryforgrowthbeforeadulthood.GHdeficienciesresultinseveregrowthdeficits,andexcessesresultingigantism.ExcessGHinadulthoodafterepiphysealclosurecausesacromegaly, characterizedbyinsidiousenlargementofthehandsandfeet,coarseningoffacialfeatures,insulinresistance,anddiabetes.GeneticdisordersoftheGH–IGF-Iaxiscauseseveregrowthimpairment.IdentifiedmutationscausingisolatedGHdeficiencymostcommonlyoccurintheGHandGHRHreceptorgenes.ThesepatientscanbetreatedwithrecombinanthGHtorestorefunctionofthedownstreamaxis.InLaronsyndrome,amutationoftheGHreceptorcausesGHresistance.InthisinstancetheliverdoesnotproduceIGF-I;thisisduetoalackofresponsivenesstoGH.ThesepatientscanbetreatedwithIGF-I,butwithoutthedirectactionsofGH,theeffectivenessofthetreatmentislimited.OtherdownstreamgeneticmutationsthathavebeenreportedincludethoseinSTAT5B,IGF-I,andALS.
The Lactotrope
The lactotrope produces the hormone prolactin, which is a 199–amino acid single-chain protein. PRL is structurally related to GH and hPL (see ). Like GH, the PRL receptor is a member of the cytokine family coupled to the JAK/STAT signaling pathways. Because the primary action of PRL in humans is related to breast development and function during pregnancy and lactation, the regulation and actions of prolactin will be discussed in detail in
In the context of the pituitary gland, it should be appreciated that the lactotrope differs from the other endocrine cell types of the adenohypophysis in two major ways: 1.
The lactotrope is not part of an endocrine axis. This means PRL acts directly on nonendocrine cells (primarily of the breast) to induce physiological changes.
2.