Humanin (Mitochondria-derived peptide (MDP))- 10MG per vial

Clinical Test Expectation – Humanin – Human Subjects : Combats necrosis of the body cells (aging). Combats Proteopathy. Neuroinflammation. Excitotoxicity. Combats obesity and weight gain. Protects the eyes. May fight Spinocerebellar Ataxia and Huntington’s Disease. Prevents chemotherapy-induced damage. Protects the vascular system. Combats obesity and weight gain. Protects against insulin resistance
Strength – 10MG per vial

Introduction
The discovery of humanin, a novel, mitochondrial-derived peptide, has created a potentially new category of biologically active peptide. As more research unravels the endogenous role of humanin as well as its potential pharmacological use, its role in stress resistance has become clearer. Humanin protects cells from oxidative stress, serum starvation, hypoxia, and other insults in vitro and also improves cardiovascular disease as well as Alzheimer’s disease in vivo. In this review, we discuss the emerging role of humanin in stress resistance and its proposed mechanism of action.

Humanin was the first smORFs to be discovered in the mtDNA, associated to a survival state in cerebral cells from Alzheimer disease. It is transcript in a mitochondrial genic region known as 16S rRNA or MT-RNR2. Structurally, Humanin is a 24 amino acid peptide, expressed in many tissues and it can be found in the blood stream of both rodents and human beings, presenting an expression decline related to the increase of age.

Two interesting studies point the ways cellular death caused by Alzheimer disease can be avoided. A study of Ikonen et al., showed that Humanin interacts with the insulin-like growth factor binding protein 3 (IGFBP-3) in rodents. IGFBP-3 belongs to a group of families responsible for transporting insulin-like growth 1 (IGF-1) and has many physiological actions independent from this transportation, such as proliferation, death and cellular survival [26,27]. Interacting with this protein, Humanin can block the induced cellular death by IGFBP-3 in cells, working as a protector effect.

Besides that, Humanin is able to interact with BAX, a key protein in the apoptosis process, avoiding its translocation to the mitochondria, suppressing the signaling cascade of apoptosis.

The levels of Humanin decrease with the aging and studies in human muscle samples showed that older subjects have a drop in total mitochondrial mass. These changes in quantity and molecular mitochondrial products can increase the sarcopenia case, with the root of other functional loses, such as mobility, independence, breathing, metabolic, etc., being physical activity as one important non-pharmacological tool to delay such events.

Few studies were developed regarding this issue. In our research we find a single study that investigated the Humanin response to the intervention of physical exercise. In this study the authors Gidlund et al. investigated the effects of resistance training (RT) in subjects with disfunction in the regulation of glucose levels. The RT was done for the great muscle groups in a periodizing linear model, with increase of weights over the course of weeks, reaching the weight of 80-90 % of a maximum repetition (1RM) in the last two weeks. Besides this protocol, the authors also investigated the effect of the cyclical cardio exercise of Nordic walking, which involves the use of canes, in an also linear periodizing, using as intensity parameter the reserve cardiac frequency, reaching 75% of this variable in the last two weeks. To both protocols, the time used for the activities was 60 minutes three times a week. The authors investigated the serum and muscle levels of Humanin, as well as the genic expression 16S rRNA (MT-NRN2) which contains the open reading structures for Humanin transcription. In this intervention model, the authors found a significative increase of Humanin muscle content level in the RT group and corelated this result to a better tolerance to glucose in this group, indicating an endocrine Humanin effect.

In this sense, Muzumdar et al. also found positive effects of Humanin administration in Diabetic animal models. The authors conclude that Humanin and its analogues have a therapeutic potential to better insulin action.

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