Mimicking Hibernation And Preserving Organs
Hibernation induction trigger (HIT) is a hormone that binds to delta-opioid receptors and has the ability to protect tissues from death, oxygen loss, and more. R
HIT may be beneficial for preserving muscle in those who are bedridden and may be useful for astronauts who are weightless. R
What Are Hibernation Induction Triggers?
Torpor is a physiological state characterized by controlled lowering of metabolic rate and core body temperature, allowing substantial energy savings during periods of reduced food availability or harsh environmental conditions. R
Hibernation is a biological strategy used to tolerate stress of depleted energy stores, intracellular acidosis, hypoxia, hypothermia, cell volume shifts, and inactivity induced muscle wasting. R
Hibernation Induction Trigger (HIT) is a hormone trigger that activates hibernation's protective mechanisms, may be an intervention for multiple stresses including environmental toxins, disease states, trauma, and aging.
In animals, HIT is able to enact hibernation/torpor, while in humans it appears to enhance survival of tissues and organs. R
What Defines A Hibernation Mimetic?
Benefits Of Hibernation Mimetics
In real life examples, hibernation mimetics should help cold, hunger, and loss of blood oxygen/glucose to cells.
Some other benefits of hibernation mimetics may be:
List Of Hibernation Mimetics
Mechanism Of Action
Some Genes HIT Should Regulate:
The delta 2 opioid receptors, DADLE and Deltorphins are mimetics of HIT and here are some of their benefits.
DADLE (D-Ala2-D-Leu5 enkephalin):
- Activates the beneficial recompensatory phase R
- Ameliorates neuronal damage induced by ischemia-reperfusion R
- Induces hibernation in hela cells R
- Protects against neurotoxins (protects dopaminergic system from methamphetamine use) R
Deltorphin D (Delt D):
- Facilitates recovery from moderate (~30%) hemorrhage after blood pressure crash R
- Has anti-inflammatory activity: Suppress LPS-induced p38 MAPK, TNFalpha. and MIP-2 R
- Induces tolerance to cardiac ischemia (via PKC, NOS, KATP channels, and the autonomic nervous system) R
Deltorphin E (Delt E):