HGH and Diabetes: What Does the Science Say?

Growth hormone is a naturally occurring peptide hormone produced by the anterior lobe of the pituitary gland. It is an anabolic hormone important for growth, cell regeneration, cell reproduction, muscle growth, burn fat, and boost metabolism.



HGH is a glucose counter-regulatory hormone, rising in response to decreased glucose in the body, it has both intrinsic hyperglycemic action and is shown to cause resistance to the action of insulin, but it is not as straight forward as it may seem.

The interplay of Hormones In Glucose Regulation

Glucose balance in circulation is tightly maintained within normal range by dynamic regulation of both glucose production from liver and kidney and glucose uptake by peripheral tissues including the liver, muscle, fat, and kidney. 

Insulin is a peptide hormone produced by Beta cells of Pancreatic Islets of Langerhans. It is the key regulator of this glucose balance in the body. It lowers postprandial (after meal) blood glucose level by increasing glucose uptake and usage from peripheral tissues of the body. It decreases the amount of gluconeogenesis and glycogenolysis.

Secretion of growth hormone is inhibited in the fed state of metabolism and its actions on glucose metabolism are mainly important during the fasting state.

There is evidence that during the fasting stage of metabolism, muscle uptake of glucose is suppressed and gluconeogenesis is potentiated  by the GH causing more glucose to be present in the bloodstream

Role of Excess GH in Diabetes

Under pathological conditions of HGH excess (acromegaly, pituitary tumors, or intake of excess exogenous GH ) these diabetogenic properties of GH become apparent. These patients show increased endogenous glucose production, decreased muscle glucose uptake which leads to excess glucose being accumulated in blood consequently.

In these patients, if their beta-cell function is intact, it produces very high amounts of Insulin (Hyperinsulinoma)  from the pancreas to counteract the excess glucose present in the blood; which on further stimulation with insulin shows resistance to insulin action.

HGH therapy in deficient cases antagonizes insulin’s action on peripheral tissues, such as the skeletal muscle, liver, and adipose tissue.

It causes increased glucose production from the skeletal muscle and liver and decreased glucose uptake from adipose tissue cells. 

Growth Hormone induced lipolysis in the adipose tissue and subsequent increased circulating FFA also interferes with insulin signaling pathways, and chronic exposure to high FFA may exert direct toxicity in beta-cells and decrease insulin sensitivity.

Hence forming the basis for the development of HGH being linked as being the cause of DM-II (Insulin Resistant Diabetes Mellitus).

However, one of the key aspects of human growth hormone (HGH) is its activation of Insulin-Like Growth Factor or IGF-.1. This chemical is closely tied to the structure and function of insulin. Also known as Somatomedin C this peptide hormone is produced from the liver and muscles in response to Growth hormone stimulation. The effects of GH on systemic glycemic control are complex partly due to this indirect activation of insulin-like growth factor 1 (IGF-1), which has glucose-lowering effects similar to insulin; producing effects opposite to that of the growth hormone.

For instance, adults with HGH deficiency are paradoxically associated with abdominal obesity and insulin resistance, which may be partly associated with their reduced IGF-1 action. Therefore we can see the net effects of GH on glucose metabolism are complicated by IGF-1 effects. The receptors for IGF-1 and insulin strongly activate their respective receptors, but can also bind and weakly activate each other’s receptors.

Studies Illustrating HGH and IGF-1’s hypoglycemic effect

In previous in vivo studies conducted, IGF-1 had caused a hypoglycemic effect through stimulation of glucose uptake into peripheral tissues and inhibition of gluconeogenesis, possibly either via activation of IGF-1 or via insulin receptors. IGF-1 has insulin-mimetic actions in the skeletal muscle and liver and increased circulating IGF-1 after HGH administration may have beneficial effects on insulin resistance and glucose metabolism.

Some studies raised concerns over increased insulin resistance and impaired fasting glucose during HGH treatment, especially in patients with obesity and elderly patients. Studies in children and adolescents also suggested that GH administration may induce insulin resistance in short-term treatment, but its long-term consequences have not been fully determined yet. Various cohort studies indicate that HGH injections may increase the incidence of type 2 diabetes mellitus in children and adolescents with predisposing risk factors, therefore it is necessary to monitor any possible negative consequences on glucose metabolism during and after GH administration.

Studies have shown children with HGH deficiency taking exogenous growth hormones are six times as likely to develop Type 2 diabetes when compared to children not taking the hormone. The result of this study stresses the importance of screening to rule out risk factors before giving growth hormones. The possibility of diabetes developing during growth hormone treatment should always be discussed with parents, and if diabetes does develop the hormonal management may be stopped or the dose can be adjusted so as not to interfere with diabetes.

Studies have shown IGF-1 to reduce the severity of diabetic retinopathy in people with Type-1 DM, whereas HGH is known to hasten the severity of retinopathy in diabetics.

The problem however in interpreting almost all human studies of IGF-1 has been that not only does it mimic and enhance insulin action, it also suppresses HGH secretion Therefore it has been difficult to discern the relative roles of the direct actions of IGF-1 and those that are mediated by suppression of GH.

One exception to this ambiguity is the group of individuals with GH receptor mutations rendering the receptors unresponsive to HGH, who develop insulin resistance as adults. Administration of IGF-1 to these patients results in an improvement in insulin sensitivity, showing direct action in blood glucose regulation; suggesting direct actions of IGF-1 rather than indirect suppressive action in response to GH excess.

Does Growth Hormone supplementation cause Diabetes?

To know exactly if Growth hormone causes Diabetes or not, it is necessary to correctly understand the functions of Somatomedin C (IGF-1); and recognize if its functions of mimicking insulin-like action are independent of its own or are only as an antagonizing action to growth hormone. If the actions of IGF-1 could be confirmed to be independent of HGH in blood glucose maintenance, the use of HGH could be attributed to causing Diabetes mellitus, but it would require many studies to be conducted on this particular topic but till then we can not say for sure that HGH results in diabetes.


Effect of Insulin-Like Growth Factor-1 on Diabetic Retinopathy in Pubertal Age Patients With Type 1 Diabetes

Effects of growth hormone on glucose metabolism and insulin resistance in human

Effects of growth hormone on glucose metabolism

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  1. James Luden Lindsay
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