Denmark also known as HN is a peptide associated with mitochondria. HN is made up of a 24 amino acid chain. Since its discovery, a decade ago Humanin has been researched in many processes such as apoptosis, substrate metabolism, cell survival and inflammatory response. Other biological processes Humanin has been reported for are response to ischemia, oxidative stress, and starvation. HN has some beneficial effects on age-related ailments including strokes, Alzheimer’s disease, diabetes, and some types of cancer, in vivo and in vitro.

Humanin has proven effects on metabolism, cell survival, inflammation in vitro and in vivo, and response to stressors. HN levels can be measured in cerebrospinal fluid, plasma, and seminal fluid.

It is thought that mitochondria are derived from bacteria that fused synergistically as a cell membrane in our cells for better utilization of energy. Throughout this process mitochondria loses a large amount of their DNA, however, holds onto the important clone sequences in DNA to encode MDPs (Mitochondria Derived Peptides).

Mitochondria Derived Peptides are important so the stability and communication of mitochondrial and cellular processes by performing on MAMs (Mitochondrial-Associates Membranes).

Humanin is a noticeable MDP that plays a significant role in regulating and signalling MAMs between the Endoplasmic Reticulum (ER) and mitochondria.

How are levels of Humanin in Your body effected Denmark?

Lowered Humanin Levels:
• Alzheimer’s Disease
• Aging (Can reduce humanin levels by up to 50%)
• Diabetes
• Mitochondrial Dysfunction
• Insulin Resistance
• Stress Response
• Vision Loss
• Vascular Dysfunction
• Elevated Humanin Levels:
• Some Cancers
• Pre-Eclampsia

What benefits does Humanin have to offer?

Better Mitochondrial Function.

Mitochondria are more vulnerable to oxidative damage such as ROS (Reactive Oxygen Species).

The mitochondrial membrane is inhibited by HN (humanin) directly, thereby protecting mitochondria from death.

HN can inhibit the release of the release of mitochondrial cytochrome and increase their production (ATP).

Humanin Denmark increases the levels of GSH (Glutathione) as well.

HN helps to prevent MELAS (Mitochondrial Encephalopathy, Lactic Acidosis, and Stroke-like Episodes.

Protects Cells From Decaying

HN can also prevent oxidative stress in cells.

Humanin Denmark improves the survival of cells by inhibiting and binding to IGFBP-3 Insulin-like Growth Factor and Bcl2-Associated X proteins (Bax).

HN can also encourage cell survival by binding and disabling the truncated BH3 protein form (tBid) and Bim isoform proapoptotic proteins (BimEL).

May Improve Longevity

GH or Growth Hormone regulates HN levels negatively.

Mice who could not produce sufficient quantities of GH, for example, had higher HN levels and lived longer than normal mice.

Centennial children have HN levels 3x higher than controls.

By suppressing the Insulin-like Growth Factor 1 (IGF-1) levels, HN may act as Calorie-restriction mimetic.

Humanin has similar traits to IGF-1 (see the above section):

  • Activate ERK1/2
  • Cardioprotective
  • Activate JAK2-STAT3
  • Controls cell death, metabolism, and transcription
  • Activate PI3K/Akt (helps with stroke)
  • Degrading Atherosclerotic Plaques
  • Enhancing Insulin Sensitivity
  • Enhance Brain Aβ Clearance
  • Lowering Inflammation
  • Found in Mitochondria, plasma, cells, skeletal muscle, liver, fat, and hypothalamus
  • Suppressing Hypoxia
  • Inhibiting Cell death

Although the longevities and growth of cancer are affected differently by HN and IGF-1, the expression of ageing has declined in both.

HN protects, for example, from cell senescence (aging of a cell biologically).

Improves Short-Term Cell Memory

HN can provide protection of brain cells against cell death induced by amyloid-beta (AB) and raise clearance levels of Alzheimer’s disease, a common Alzheimer’s disease pathology (AD).

HN can also prevent Tau hyperphosphorylation in the brain (an AD pathology).

Humanin may enhance memory.

For example, in important mechanisms used to form memory, HN can also reverse Long-Term Potentiation (LTP) loss from AB.

HN may stop other anticholinergic medicines memory loss as well.

Scopolamine, for example, a Muscarinic Acetylcholine Receptor antagonist (mAChR) is a standard for testing AD animal models and can cause short memory loss.

The short-term memory loss from scopolamine can be reversed by a modified version of HN called HumaninG (HNG).

The neuroprotective effects of HN have been increased to 1000-fold by this amendment (HNG).

Intranasally taken, HNG can reduce AB accumulation and reduce AD animal model memory deficit.

HN may protect the principal pathology of type 3 Alzheimer’s/diabetes, Insulin Resistance (IR), in the brain.

HN is a strong insulin sensitizer, for example, and can help with IR in DC by stimulating STAT3 and inhibiting IGFBP3 in hypothalamus.

HNG can improve autophagy on the hippocampus with the regulation of IRS-1/mTOR signals.

HN offers neuroprotection against a number of family Alzheimer’s (FAD) genes, including preseniline 1, presenilin 2, and Amyloid Precursor Protein Mutated (APP).

HN is also binding for neurodegenerative disease, spinal cord injuries, retinal degeneration, autoimmune neuroinflammation and metabolic disease-related obesity-related illnesses with the Ciliary Neurotrophic Factor receptor (CNTF).

Combat Protection, Neuroinflammation, And Excess Toxicity

Calcium efflux leading to proteopathy (toxic depleted/maligned protein aggregates) occurs in the endoplasmic reticulum (ER).

In two ways, HN protects from proteopathy:

ROS formation can be inhibited by HN

Calcium release may be inhibited by HN

HN can protect it from prion-proteopathy, for example.

Humanin Denmark also protects against neuroinflammation caused by lipopolysaccharide (endotoxemia).

It will also prevent excitotoxicity (both via action on NMDARs and independently).

For example, HN may prevent excitotoxicity caused by the overactivation of NMDA receptors from reactive oxygen (ROS) species and nitrous oxide (NOs).

Lactate dehydrogenase (LDH) in the brain may also be reduced by HN.

Protects From Resistance To Insulin

In non-obese diabetically animal models, HN is able to inhibit pancreatic beta-cell death and increase glucose tolerance.

This can be beneficial both for Type 1 and Type 2 diabetes (T2D).

HN can also improve the sensitivity to insulin in the liver and stabilise the levels of blood glucose through action on the hypothalamus.

For quicking glucose-related stresses, HN can be a good biomarker.

Triglyceride (TG) secretion from the liver is increased acutely by HNG.

Combats Weight Gain And Obesity

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By increasing glucose-reduced release and reducing body weight gain and visceral fat, HN may prevent weight gain.

Helps To Protect Your Eyes

The degeneration of the retina from oxidative stress is caused through the age-related degeneration of the macular degeneration (AMD).

In order to prevent retinal pigment epithelium (RPE) in AMD, mitochondrial ER plays a huge role.

HN and HNG prevent both AMD and RPE’s cell death by increasing mitochondrial levels of GSH and lowering the ROS, caspase 3, and caspase 4. HN and HNG prevent both AMD and cell death.

May Fight Ataxia and Huntington Disease of Spinocerebellar

Polyglutamine toxicity (PolyQ) is characterised by spino-cervical ataxia (SA) and Huntington’s disease (HD).

HN can prevent mitochondrial dysfunction caused by PolyQ.

May Aid With Lateral Amyotrophic Sclerosis

HN may assist Family Lateral Amyotrophic Sclerosis (ALS).

For example, the dose-dependent improved motor performance and prolonged surviving ALS mice of animal models with G93A-SOD1 mutations.

Could Protect Skin Against Sunburn

HN can protect against induced cell death caused by Ultraviolet (UV).

Shields The Cardiac System 

Patients with atherosclerotic plaques were shown to have high HN levels and could protect themselves from atherosclerosis.

HNG was able to enhance cardiovascular function from high cholesterol diets in animal models, for example (a plaque-reduction of ~ 90%) that failed to express APOE (a key protein for cholesterol metabolism).

HN can protect HN cells against oxidising stress caused by oxidised LDL (oxLDL).

Increasing AMPK and eNOS can protect the HNG from coronary occlusion damage, reducing the sizes of the infarct and oxidative stress during a heart attack.

Shields Against Ischemia And Hypoxia

The stresses of hypoxia and ischemia can be reduced by HN.

HNG is neuroprotective during hypoxia by activating PI3K/Akt and Jak2/Stat3.

For instance, HN can protect against compound cobalt chloride (CoCl2) induced cellular hypoxia.

The copper chelator, Cuprizone (CPZ) causes demyelination, and symptoms similar to schizophrenia.

HN is able to eliminate neuroinflammation and CPZ cognitive impairments.

The axonal remiolation in the hypoxic brains has proved to be caused by HN.

One of the biggest problems with ischemia is blood flow loss, which reduces growth factors, leading to cell mortality.

HN can prevent ischemic cell death and enhance hypoxic cell energy generation (ATP).

HN can also help to protect HN against ischemic and hemorrhagic stroke-induced damage in traumatic brain injury (TBI).

HNG was able to reduce the volume of infarcts by 50 percent in animal models, for example.

The upregulement of Suppressor of Cytokine 3 is one of the reasons why HNG can protect against TBI (SOCS3).

Helps Protect The Colon

HNG can protect against colon inflammation and improve weight loss in experimental models of Ulcerative Colitis (UC).

The Kidneys Are Protected From Inflammation

HN can prevent inflammation of the kidneys.

For instance, HN could protect against developing kidney disease in deficient APOE mice.

Safeguards The Male Productive System 

At all stages of development of the testis HN is present.

HN is able to protect against death against testicular and sperm cells.

Soothes Anxiety

Humanin Denmark can prevent memory impairment induced by diazepam and act as an anxiety agent. HN can prevent memory impairment.

Humanin can improve anxiety by working with the Formyl Peptide Receptor 2 (FPR2).

Prevents Damage Caused By Chemotherapy

White blood cells are protected against chemotherapy damage by HN.

In anti-cancer treatment, HNG prevents impairment of bortezomib-induced bone growth.

Sperm cells can protect HN against the death by chemotherapy of cells.

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