Somatotropin (STH)
Somatotropin (STH) or growth hormone (GH) is a complex protein having 191 amino acids and S‑S bridges. The STH is species specific and most domestic animals respond best to homologous STH and least to heterologous STH.
STH is structurally related to prolactin and chorionic somatomammotropin of the same species.
Control of Somatotropin (STH) output
The control of STH output is achieved by a balance between the growth hormone releasing hormone (GHRH) and somatostatin.
A sharp drop in blood glucose and fatty acids levels is the primary cause of GHRH release from the hypothalamus and it results in two to ten fold increases in STH secretion.
Stimuli that increases the GH secretion
Stimuli that increases the GH secretion of Somatotropin (STH) or growth hormone (GH)-
- Deficiency of energy – hypoglycaemia, exercise, fasting, insulin
- Increase in circulating levels of certain amino acids – protein meal, arginine vasopressin
- Glucagon (mechanism not known)
- Stress (trauma, surgery) pyrogen
- Sleep
- Ghrelin, a 28 amino acid polypeptide hormone secreted from hypothalamus (also from stomach) stimulates GH release
Stimuli that decreases the GH secretion
Stimuli that decreases the GH secretion of Somatotropin (STH) or growth hormone (GH)-
- Increase in glucose, cortisol, free fatty acids, GH
- Obesity results in reduced GH release
- GIH
Notes of Growth Hormone
1. STH appears to be released at a rather similar rate through out the life of the animal
2. Although skeletal growth cease after puberty, STH has a biological role throughout life as an anabolic agent as well as synergistic role by enhancing the actions of ACTH, TSH, LH, and FSH on their target organs
3. Females are more responsive to GH stimuli than males
Physiological effects of Somatotropin (STH)
Growth hormone or Somatotropin (STH) has two distinct types of effects- Direct effects are the result of growth hormone binding its receptor on target cells. Fat cells (adipocytes), for example, have growth hormone receptors, and growth hormone stimulates them to break down triglyceride and suppresses their ability to take up and accumulate circulating lipids.
Indirect effects are mediated primarily by an insulin-like growth factor-1 (IGF-1), a hormone that is secreted from the liver and other tissues in response to growth hormone. A majority of the growth promoting effects of growth hormone is actually due to IGF-1 acting on its target cells.
Normal Effects in the Body
The STH does not have a specific target organ. GH exerts its effect on almost all tissues of the body.
STH causes both increase in size (hypertrophy) and number of cells (hyperplasia), and promotes growth of all tissues of the body which are capable of growing.
GH enhances the activities of the visceral organs like liver, kidney, intestine, endocrine glands- parathyroid and pancreas. It stimulates cardiac output, glomerular filtration and the metabolic activities in liver, skeletal muscle and heart.
Increases both the soft and osseous tissues of the body and has a profound effect on lactation.
Effects on Growth
Growth is a very complex process, and requires the coordinated action of several hormones.
GH does not act directly on bone and cartilage, but indirectly by causing the liver to produce smaller proteins called somatomedinsthat act on cartilages and bone to promote their growth.
Two somatomedins, C and A have been identified which resemble structurally to insulin and hence they are also known as insulin like growth factors I and II (IGF I & II) respectively.
IGF I is transported in blood bound with specific binding proteins called IGF-binding proteins (IGFBP); this binding of IGF prolongs the half-life of IGF I.
The receptor for IGF is similar to insulin receptors. IGF I promotes skeletal and cartilage growth and IGF II is functional during foetal period.
The metabolic effects of GH on most of the cells are promoted by stimulating the liver and other tissues to secrete IGF-I or somatomedin C.
IGF-I stimulates proliferation of chondrocytes (cartilage cells) resulting in bone growth. GH also seems to have a direct effect on bone growth in stimulating differentiation of chondrocytes. Somatomedin production is inhibited by estrogen and cortisol.
IGF-I also increase muscle growth. It stimulates both the differentiation and proliferation of myoblasts. It also stimulates amino acid uptake and protein synthesis in muscle and other tissues.
Growth of the long bones continues so long as the epiphyseal lines do not close. In domestic animals, closure of epiphyseal lines soon after puberty signals the cessation of skeletal growth under normal conditions.
Metabolic effects of Somatotropin (STH)
As a protein anabolic hormone GH enhances almost all facets of amino acid metabolism including uptake, while at the same time reducing the break down of proteins. This includes transport through the cell membrane to the interior of the cells and increased protein synthesis in all cells of the body more specifically the muscle cells. It stimulates extracellular collagen deposition
Stimulates the formation of RNA by increasing the transcription process in the nucleus.
By enhancing the ribosomal machinery, produces greater number of protein molecules.
As a potent protein sparer, it causes decreased catabolism of protein and amino acids for energy. Protein content of the body is increased by GH.
It stimulates lipolysisand mobilizes large quantities of free fatty acids from the adipose tissue. It enhances the conversion of fatty acids to acetyl Co‑ A, which is used for energy. Excessive amount of STH at times causes greater amounts of fat mobilization resulting in excess acetyl Co‑A which is converted to acetoacetate, b ‑OH butyric acid and acetone leading to ketonemia which is called as ketogenic effect of GH. It reduces lipid synthesis and leads to leaner animal. GH decreases body fat content and promotes lean body mass.
GH causes decreased utilization of glucose for energy (possibly duo to utilization of fat for energy) and enhanced glycogen deposition. It diminishes uptake of glucose by the cells for energy by the muscle and adipose cells, thus increases blood glucose concentration which is known as diabetogenic effect of GH.
GH shows positive nitrogen balance and phosphorus balance. It decreases urinary excretion of Na+ and K+ by increasing the uptake of these ions by the growing tissues.
In the cow lactation can be induced with STH more easily and with greater regularity than with lactogenic hormone (prolactin). This is due to galactopoietic effect of STH
In summery, STH favours economical use of proteins and carbohydrates, encouraging the body to retain these building blocks for tissue growth and development.
Injection of growth hormone increases milk yield by 10-25%, lactose, protein and fat contents of milk. Endogenous plasma concentrations of GH are high in high yielding than low yielding animals.GH partitions nutrients for milk yield and increases fatty acid mobilisation. Exogenous GH increases nitrogen retention and improves carcass quality with improved muscle growth; helps in lean meat production with less adipose tissue in cattle, pigs, sheep.
Effects of abnormal production of Growth Hormone
Panhypopituitarismis decreased secretion of all the anterior pituitary hormones. Underproduction of pituitary hormones in the immature animal results in underdevelopment of the animal referred to as pituitary dwarfism. Such an animal shows reduced activity in the other target organs of the pituitary (hypothyroidism, hypogonadism, hypoadrenocortical function).
The effects of overproduction of STH depend to a great extent on the age of the animal in which this overproduction occurs.
If the overproduction occurs before the closure of epiphyseal lines in the long bones, it results in lengthening of the long bones and increased deposition of soft tissue, resulting in gigantism. This condition occasionally occurs in domestic animals.
If excess production of STH occurs after the closure of epiphyseal lines, the long bones of the body are thickened and there is excessive soft tissue and this condition is termed as acromegaly. This is produced in acidophilic tumours.