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Growth Hormone Tips

Growth hormone, also known as somatotropin, is a protein hormoneof about 190 aminoacids that is synthesized and secreted by cells called somatotrophsin the anterior pituitary.

It is a major participant in control of several complex physiologicprocesses, including growth and metabolism. Growth hormone isalso of considerable interest as a drug used in both humans and animals.

Last Updated - 7th November 2005

Physiologic Effects of Growth Hormone

A critical concept in understanding growth hormone activity is thatit has two distinct types of effects:

• Direct effects are the result of growth hormone binding itsreceptor on target cells. Fat cells (adipocytes), for example, havegrowth hormone receptors, and growth hormone stimulates them to breakdown triglyceride and supresses their ability to take up and accumulatecirculating lipids.
• Indirect effects are mediated primarily by a insulin-likegrowth factor-I (IGF-I), a hormone that is secreted from the liverand other tissues in response to growth hormone. A majority of thegrowth promoting effects of growth hormone is actually due to IGF-Iacting on its target cells.
  

Effects on Growth

Growth is a very complex process, and requires the coordinated actionof several hormones. The major role of growth hormone in stimulatingbody growth is to stimulate the liver and other tissues to secrete IGF-I.IGF-I stimulates proliferation of chondrocytes (cartilage cells), resultingin bone growth. Growth hormone does seem to have a direct effect onbone growth in stimulating differentiation of chondrocytes.

IGF-I also appears to be the key player in muscle growth. It stimulatesboth the differentiation and proliferation of myoblasts. It also stimulatesamino acid uptake and protein synthesis in muscle and other tissues.

Metabolic Effects

Growth hormone has important effects on protein, lipid and carbohydratemetabolism. In some cases, a direct effect of growth hormone has beenclearly demonstrated, in others, IGF-I is thought to be the criticalmediator, and some cases it appears that both direct and indirect effectsare at play.

• Protein metabolism: In general, growth hormone stimulatesprotein anabolism in many tissues. This effect reflects increasedamino acid uptake, increased protein synthesis and decreased oxidationof proteins.
• Fat metabolism: Growth hormone enhances the utilization offat by stimulating triglyceride breakdown and oxidation in adipocytes.
• Carbohydrate metabolism: Growth hormone is one of a batteryof hormones that serves to maintain blood glucose within a normalrange. Growth hormone is often said to have anti-insulin activity,because it supresses the abilities of insulin to stimulate uptakeof glucose in peripheral tissues and enhance glucose synthesis inthe liver. Somewhat paradoxically, administration of growth hormonestimulates insulin secretion, leading to hyperinsulinemia.
  

Control of Growth Hormone Secretion

Production of growth hormone is modulated by many factors, includingstress, exercise, nutrition, sleep and growth hormone itself. However,its primary controllers are two hypothalamic hormones and one hormonefrom the stomach:

• Growth hormone-releasing hormone (GHRH) is a hypothalamicpeptide that stimulates both the synthesis and secretion of growthhormone.
• Somatostatin (SS) is a peptide produced by several tissuesin the body, including the hypothalamus. Somatostatin inhibits growthhormone release in response to GHRH and to other stimulatory factorssuch as low blood glucose concentration.
• Ghrelin is a peptide hormone secreted from the stomach. Ghrelinbinds to receptors on somatotrophs and potently stimulates secretionof growth hormone.
  

Growth hormone secretion is also part of a negative feedbackloop involving IGF-I. High blood levels of IGF-I lead todecreased secretion of growth hormone not only by directly suppressingthe somatotroph, but by stimulating release of somatostatin from thehypothalamus.

Growth hormone also feeds back to inhibit GHRH secretionand probably has a direct (autocrine) inhibitory effect on secretionfrom the somatotroph.

Integration of all the factors that affect growth hormone synthesisand secretion lead to a pulsatile pattern of release. Basal concentrationsof growth hormone in blood are very low. In children and young adults,the most intense period of growth hormone release is shortly after theonset of deep sleep.

Disease States

States of both growth hormone deficiency and excess providevery visible testaments to the role of this hormone in normal physiology.Such disorders can reflect lesions in either the hypothalamus, the pituitaryor in target cells. A deficiency state can result not only from a deficiencyin production of the hormone, but in the target cell's response to thehormone.

Clinically, deficiency in growth hormone or receptor defectsare as growth retardation or dwarfism. The manifestation of growth hormonedeficiency depends upon the age of onset of the disorder and can resultfrom either heritable or acquired disease.

The effect of excessive secretion of growth hormone is alsovery dependent on the age of onset and is seen as two distinctive disorders:

• Giantism is the result of excessive growth hormone secretionthat begins in young children or adolescents. It is a very rare disorder,usually resulting from a tumor of somatotropes. One of the most famousgiants was a man named Robert Wadlow. He weighed 8.5 pounds at birth,but by 5 years of age was 105 pounds and 5 feet 4 inches tall. Robertreached an adult weight of 490 pounds and 8 feet 11 inches in height.He died at age 22.
• Acromegaly results from excessive secretion of growth hormonein adults. The onset of this disorder is typically insideous. Clinically,an overgrowth of bone and connective tissue leads to a change in appearancethat might be described as having "coarse features". Theexcessive growth hormone and IGF-I also lead to metabolic derangements,including glucose intolerance.
  

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Pharmaceutical and Biotechnological Uses ofGrowth Hormone

In years past, growth hormone purified from human cadaver pituitarieswas used to treat children with severe growth retardation. More recently,the virtually unlimited supply of recombinant growth hormone has leadto several other applications to human and animal populations.

• Human growth hormone is commonly used to treat children ofpathologically short stature. There is concern that this practicewill be extended to treatment of essentially normal children - socalled "enhancement therapy" or growth hormone on demand.Similarly, growth hormone has been used by some to enhance atheleticperformance. Although growth hormone therapy is generally safe, itis not as safe as no therapy and does entail unpredictable healthrisks. Parents that request growth hormone therapy for children ofessentially-normal stature are clearly misguided.
• The role of growth hormone in normal aging remains poorlyunderstood, but some of the cosmetic symptoms of aging appear to beamenable to growth hormone therapy. This is an active area of research,and additional information and recommendations about risks and benefitswill undoubtedly surface in the near future.
• Growth hormone is currently approved and marketedfor enhancing milk production in dairy cattle. There is nodoubt that administration of bovine somatotropin to lactating cowsresults in increased milk yield, and, depending on the way the cowsare managed, can be an economically-viable therapy. However, thistreatment engenders abundant controversy, even among dairy farmers.One thing that appears clear is that drinking milk from cattle treatedwith bovine growth hormone does not pose a risk to human health.

Another application of growth hormone in animal agriculture is treatmentof growing pigs with porcine growth hormone. Such treatment has beendemonstrated to significantly stimulate muscle growth and reduce depositionof fat.

Growth Hormone andAging

Normal Changes in the Growth Hormone Axiswith Aging

• The rate of GH secretion from the anterior pituitary is highestaround puberty, and declines progressively thereafter.This age-related decline in GH secretion involves a number of changesin the GH axis, including decreased serum levels of insulin-like growthfactor-1 (IGF-1) and decreased secretion of growth hormone-releasinghormone from the hypothalamus. The cause of the normal age-relateddecrease in GH secretion is not well understood, but is thought toresult, in part, from increased secretion of somatostatin, the GH-inhibitinghormone.
• Normal aging is accompanied by a number of catabolic effects,including a decrease in lean mass, increase in fat mass, and decreasein bone density. Associated with these physiologic changes isa clinical picture often referred to as the somatopause: frailty,muscle atrophy, relative obesity, increased frequency of fracturesand disordered sleep. These clinical signs of aging are, without doubt,the manifestation of a very complex set of changes which involve,at least in part, the GH-axis. Naturally, this has spurred considerableinterest in administering supplemental GH as a "treatment"for aging in humans, and the availability of recombinant human GHhas made such studies feasible.
• In contrast to the view that GH deficiency contributes to the agingphenomenon, there is information suggesting that normal orhigh levels of GH may accelerate aging. Mice with geneticdwarfism due to deficiency in GH, prolactin and thyroid-stimulatinghormone live considerably longer than normal mice, and the increasedlevels of GH seen with acromegaly in humans are associated with reducedlife expectancy. Both of these findings are likely due to metaboliceffects of GH.

GH Replacement Therapy in GH-deficient Adults

• Adult-onset GH deficiency in humans is almost always due to pituitarydisease, usually from a tumor or therapeutic efforts to treat a tumor.Such patients have increased risk of death from cardiovascular disease,and, relative to age-matched controls, show increased fat mass, reducedmuscle mass and strength, lower bone density, and higher serum lipidconcentrations. Additionally, they suffer from reduced vigor, sexualdysfunction and emotional problems.
• More than a dozen clinical trials have sought to evaluate GH replacementin patients with adult-onset deficiency. The goal has usually beento normalize serum IGF-1 concentrations by daily injections of GH.In essentially all cases, several months of GH replacement therapyled to increased lean mass and decreased adiposity (especially invisceral fat). The effects of GH treatment on bone density and hyperlipidemiahas been inconsistent or minor, as have been the effects on strengthand mental abilities. Common side effects observed in these trialsincluded edema and joint/muscle pain, which appeared related to doseof GH. Since the first of these trials was conducted in 1988, longterm risks are not yet known.

GH Therapy in the Elderly

In 1990, considerable excitement was generated from a report by Rudmanand colleagues which described wonderful effects of GH treatment ina small group of elderly men. These volunteers, who ranged in age from61 to 81 years, showed increased lean body and bone mass, decreasedfat mass and, perhaps most dramatically, restoration of skin thicknessto that typical of a 50-year-old.

The study cited above and a handful of others have provided an initialunderstanding of the benefits, limitations and risks of sustained (6to 12 month) GH supplementation in elderly men and women. A consistentfinding in these investigations was a high incidence of adverse sideeffects - edema, fluid retention and carpal tunnel syndrome - whichnecessitated reductions in GH dose of cessation of treatment. GH treatmentconsistently induced an increase in serum IGF-1, a decrease in fat massand increase in lean mass.

The effects on fat and lean masses may be viewed as positive effects,but, at the end of the day, it has to be asked whether GH treatmentimproved functioning in the elderly. In the studies in which functionwas objectively assessed, GH treatment did not improve cognitive function,and, despite the effects on lean body mass, was not any more effectivethan exercise alone in promoting strength. Long-term GH therapy in elderlypostmenopausal women lead to significant increases in bone mineral density,but these increases were less than what is routinely achieved with estrogenreplacement. While it must be acknowledged that a relatively small numberof elderly patients have been treated for prolonged periods with GH,the controlled trials conducted thus far do not support is efficacyin aleviating age-related deficits in cognitive or somatic function.

Another indication of potentially serious side effects of GH therapyin adults, including the elderly, has been provided by controlled clinicaltrials that assessed the utility of human GH treatment in critical illness,where endogenous GH secretion is typically suppressed. GH therapy wasanticipated to attenuate the catabolic effects of illness and therebydecrease duration of hospitalization. The results of several clinicaltrials involving hundreds of patients, demonstrated a significant increasein mortality associated with high doses of GH. Additionally, those patientstreated with GH that survived had longer periods of intensive care andhospitalization than those receiving placebos.

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