Ipamorelin

Ipamorelin Research

Ipamorelin is a synthetic peptide that functions as a growth hormone secretagogue – it stimulates the release of growth hormone from the pituitary gland. As a pentapeptide (made of five amino acids), it works by mimicking the action of ghrelin (often called the “hunger hormone”) in the body.

Key characteristics of Ipamorelin include:

• Considered a “selective” growth hormone secretagogue, meaning it stimulates growth hormone release without significantly affecting other hormones like cortisol or prolactin
• Used in research settings or prescribed off-label for conditions related to growth hormone deficiency
• Studied for potential applications in muscle recovery, fat loss, sleep quality, and tissue repair

Muscle Tissue Preservation

Ipamorelin has demonstrated potential in counteracting muscle wasting. In a study involving glucocorticoid-treated rats, which typically experience muscle and bone degradation, ipamorelin administration significantly increased muscle strength and bone formation rates5.

This suggests that ipamorelin can mitigate the catabolic effects of glucocorticoids on muscle tissue, thereby preserving muscle function and structure.

Growth Hormone and Body Composition

Ipamorelin’s mechanism of action is similar to that of growth hormone-releasing hormone but does not lead to desensitization of the growth hormone response2.

Ipamorelin has been shown to increase body weight in both growth hormone-deficient and intact mice, with a notable increase in fat pad weights relative to body weight. This suggests that ipamorelin may promote fat accumulation through mechanisms independent of growth hormone1.

In young female rats, chronic ipamorelin treatment resulted in higher weight gain compared to controls, indicating its potential to enhance body weight2.

Treatment with ipamorelin increased relative body fat in growth hormone-intact mice, as measured by dual-energy X-ray absorptiometry (DEXA). Additionally, it elevated serum leptin levels and food intake, which may contribute to increased adiposity1.

In adult female rats, ipamorelin increased bone mineral content, although the increase was attributed to greater bone growth rather than changes in bone density3.

Bone Growth and Development

Ipamorelin increases bone mineral content (BMC) in adult female rats. This increase is attributed to enhanced bone growth and dimensions, although the volumetric bone mineral density (BMD) remains unchanged3. The treatment with ipamorelin results in increased cortical BMC due to a larger cross-sectional bone area, while the mineral concentration within the bone does not change3.

Ipamorelin induces a dose-dependent increase in longitudinal bone growth rate (LGR) in rats. This effect is accompanied by a significant gain in body weight, although it does not alter total IGF-I levels or serum markers of bone formation and resorption4.

Ipamorelin can counteract the negative effects of glucocorticoids on bone formation. In rats treated with both glucocorticoids and ipamorelin, there is a significant increase in periosteal bone formation rate compared to those treated with glucocorticoids alone5.

Gastrointestinal Health

Ipamorelin functions by binding to the ghrelin receptor, which is present in various tissues including the gastrointestinal tract. This binding stimulates the release of growth hormone and enhances gastric motility, potentially improving conditions like postoperative ileus (POI) and gastroparesis6.

Diabetic Models

Ipamorelin has been shown to significantly increase insulin secretion from the pancreas in both normal and diabetic rats. This effect is mediated through calcium channels and adrenergic receptor pathways. The presence of certain inhibitors, such as diltiazem, yohimbine, and propranolol, can significantly reduce this insulin release, indicating the involvement of these pathways in ipamorelin’s action. Notably, atropine specifically reduced insulin secretion in diabetic rats, suggesting a differential mechanism in diabetic conditions7.

In streptozotocin (STZ) diabetic mice, ipamorelin administration resulted in increased growth hormone levels compared to nondiabetic mice. However, these diabetic mice exhibited GH resistance, as indicated by unchanged IGF-I mRNA levels and peptide expression in the liver, despite the elevated GH levels. This suggests that while ipamorelin can stimulate GH secretion, the downstream effects on the GH/IGF-I axis are impaired in diabetic conditions8.

References