Oxytocin is a 9-amino acid neuropeptide hormone produced in the hypothalamus and secreted by the posterior pituitary gland. It plays a crucial role in various physiological processes, including uterine contractions during labor, milk ejection during breastfeeding, and modulation of social behaviors such as bonding and trust. The 2 mg formulation refers to the lyophilized (freeze-dried) powder form of oxytocin, intended for reconstitution and research applications.
Oxytocin can modulate inflammation by acting on specific inflammatory cytokines. An interesting study involving 37 couples found that social interaction, which elevated oxytocin levels, significantly increased wound healing rates. The higher the oxytocin levels, the faster the wounds healed. Conversely, hostility in interpersonal relationships, especially among couples, was found to reduce wound healing rates by up to 40%. These hostile couples also exhibited lower levels of IL-6, tumor necrosis factor-alpha, and IL-1beta at the wound site.
Given its ability to enhance wound healing and regulate inflammatory cytokines, researchers hypothesized that oxytocin may also protect the heart and vascular system. Oxytocin has been shown to reduce fat mass, improve glucose tolerance, lower blood pressure, and relieve anxiety. All of these factors play significant roles in cardiovascular disease (CVD), suggesting oxytocin might serve as a valuable adjunct to current CVD therapies.
There is substantial evidence that atherosclerosis in some cases results from suppressed oxytocin receptor expression. Increasing oxytocin levels in individuals with reduced receptor density may help maintain cardiovascular integrity and, in certain instances, reverse atherosclerosis.
Research in rats suggests that oxytocin infusion directly into the heart during ischemic events (e.g., heart attacks) protects cardiomyocytes from death. Chronic oxytocin treatment may prevent late-stage dilated cardiomyopathy and could precondition cardiac stem cells to promote tissue regeneration through differentiation, secretion of protective factors, or fusion with injured cardiomyocytes. Additional studies in diabetic mice demonstrate that oxytocin reduces body fat by 19% and lowers fasting glucose by 23%, likely by decreasing insulin resistance. Treated mice exhibited less systolic and diastolic dysfunction, resulting in reduced cardiomyocyte hypertrophy, fibrosis, and apoptosis.
Oxytocin’s protective effects against ischemic injuries extend beyond the heart. For example, in rats with priapism (persistent erection), oxytocin administration reduced ischemia-reperfusion injury by lowering nitric oxide levels.
Oxytocin likely enhances glucose uptake in skeletal muscle by improving insulin sensitivity, making it a potential diabetes treatment. Research in mice also shows oxytocin’s role in lipid metabolism, reducing total body fat and dyslipidemia. Oxytocin deficiencies have been linked to obesity despite normal diet and exercise, indicating its critical role in energy balance.
Interestingly, oxytocin treatment affects glucose, insulin, and body composition in obese but not lean mice, suggesting its therapeutic effects may be limited to specific diabetic contexts. In diabetic patients, intranasal oxytocin reduced glucose and insulin levels and resulted in an average 9 kg weight loss over eight weeks. Circulating oxytocin levels are lower in type 2 diabetes patients and negatively correlate with HbA1c and insulin resistance.
Early maternal deprivation can cause lasting cognitive and behavioral impairments, possibly due to oxytocin changes caused by reduced parental bonding. In one study, maternally deprived mice treated with oxytocin showed improved levels of neuron development hormones in the prefrontal cortex. Although behavioral improvements were not statistically significant, trends favored the oxytocin group. Other research similarly found intranasal oxytocin modestly improved learning under stress.
Extensive evidence links oxytocin to anxiety and depression. Genetic polymorphisms in the oxytocin receptor gene can cause social anxiety disorder and childhood attachment issues. In untreated social anxiety patients, epigenetic changes in the oxytocin receptor suggest compensatory mechanisms for reduced oxytocin signaling. This implies social anxiety may partly arise from diminished oxytocin activity.
Borderline personality disorder (BPD), an extreme social anxiety form, is associated with oxytocin dysregulation. BPD involves hypervigilance, mistrust, and altered social behaviors. Intranasal oxytocin administration modifies these behaviors, offering a rare insight into a difficult-to-treat condition affecting many lives.
Research on Prader-Willi syndrome—a condition characterized by uncontrollable appetite—reveals that excessive suppression of oxytocin signaling contributes to the disorder. There is increasing evidence that oxytocin regulates hunger states and directly influences feeding behavior.
New findings show oxytocin is essential for healthy muscle maintenance and repair. Age-related declines in oxytocin signaling contribute to sarcopenia (muscle wasting). Research at Berkeley demonstrated that as blood oxytocin and muscle stem cell receptor levels drop with age, muscle repair capacity diminishes. Remarkably, oxytocin administration reverses these declines within days, restoring muscle healing potential to about 80% of that seen in young mice. This suggests oxytocin may offer interventions to slow age-related organ degeneration.
Research Applications
Oxytocin 2 mg is utilized in scientific studies focusing on:
Product Specifications
Safety and Handling
Oxytocin 2 mg is intended strictly for laboratory research and is not approved for human consumption. Handle with care, following appropriate safety protocols. Ensure proper storage conditions to maintain the integrity and efficacy of the compound.
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