Nitric oxide receptor enzyme
Soluble guanylate cyclase (sGC)
Also searched as Soluble guanylate cyclase (sGC).
The messenger that carries the second fat-release road can be made two ways. Made at the heart-peptide receptor, it releases fat. Made by the nitric-oxide enzyme, it does the reverse: blocking nitric oxide raised fat release in living people, and supplying it lowered release in isolated fat cells — with the blood-flow explanation ruled out in the same experiment. It also favors the formation of new fat cells. The practical rule: something that raises nitric oxide is not a fat-release agent, however good it is for circulation. Those two effects are separable and they point opposite ways.
In depth
A second enzyme that makes the same messenger — and in fat cells produces the opposite result.
What drives it
Blood flow (nitric oxide) increases it.
Two different enzymes make the same messenger, and in fat they do opposite things. This is the most counter-intuitive finding on this MAP and it overturns the obvious assumption. The messenger made at the heart-peptide receptor releases fat. The same messenger made by the nitric-oxide enzyme does the reverse. Measured in living people, not in cells: 'the NO synthase inhibitor, L-NMMA, but not the biologically inactive enantiomer, increased glycerol levels in the microdialysates without causing a change of local blood flow... Nitric oxide gas as well as the NO donor, NITROGLYCERINE, reduced glycerol release from isolated adipocytes' (PMID 10323597 — a nitric oxide-mediated mechanism regulates lipolysis in human adipose tissue in vivo (microdialysis)). ⇒ blocking nitric oxide raises fat release. Supplying it lowers fat release. And the blood-flow explanation is ruled out in the same experiment. It also favors fat cell formation: 'nitric oxide and downstream second messenger cGMP and cAMP enhance adipogenesis in primary human preadipocytes' (Cytotherapy 2010 — Nitric oxide and downstream second messenger cGMP and cAMP enhance adipogenesis in primary human preadipocytes). The practical rule this establishes: a compound that raises nitric oxide is not a fat-release agent, however good it is for blood flow. The two effects are separable and they point in opposite directions. The field itself is cautious: 'the effect of nitric oxide appears complex and is not fully understood'. PMID 10323597
What it drives
It increases Vasodilation signal.
Two different enzymes make the same messenger, and in fat they do opposite things. This is the most counter-intuitive finding on this MAP and it overturns the obvious assumption. The messenger made at the heart-peptide receptor releases fat. The same messenger made by the nitric-oxide enzyme does the reverse. Measured in living people, not in cells: 'the NO synthase inhibitor, L-NMMA, but not the biologically inactive enantiomer, increased glycerol levels in the microdialysates without causing a change of local blood flow... Nitric oxide gas as well as the NO donor, NITROGLYCERINE, reduced glycerol release from isolated adipocytes' (PMID 10323597 — a nitric oxide-mediated mechanism regulates lipolysis in human adipose tissue in vivo (microdialysis)). ⇒ blocking nitric oxide raises fat release. Supplying it lowers fat release. And the blood-flow explanation is ruled out in the same experiment. It also favors fat cell formation: 'nitric oxide and downstream second messenger cGMP and cAMP enhance adipogenesis in primary human preadipocytes' (Cytotherapy 2010 — Nitric oxide and downstream second messenger cGMP and cAMP enhance adipogenesis in primary human preadipocytes). The practical rule this establishes: a compound that raises nitric oxide is not a fat-release agent, however good it is for blood flow. The two effects are separable and they point in opposite directions. The field itself is cautious: 'the effect of nitric oxide appears complex and is not fully understood'. PMID 10323597
It reduces Releases stored fat.
Two different enzymes make the same messenger, and in fat they do opposite things. This is the most counter-intuitive finding on this MAP and it overturns the obvious assumption. The messenger made at the heart-peptide receptor releases fat. The same messenger made by the nitric-oxide enzyme does the reverse. Measured in living people, not in cells: 'the NO synthase inhibitor, L-NMMA, but not the biologically inactive enantiomer, increased glycerol levels in the microdialysates without causing a change of local blood flow... Nitric oxide gas as well as the NO donor, NITROGLYCERINE, reduced glycerol release from isolated adipocytes' (PMID 10323597 — a nitric oxide-mediated mechanism regulates lipolysis in human adipose tissue in vivo (microdialysis)). ⇒ blocking nitric oxide raises fat release. Supplying it lowers fat release. And the blood-flow explanation is ruled out in the same experiment. It also favors fat cell formation: 'nitric oxide and downstream second messenger cGMP and cAMP enhance adipogenesis in primary human preadipocytes' (Cytotherapy 2010 — Nitric oxide and downstream second messenger cGMP and cAMP enhance adipogenesis in primary human preadipocytes). The practical rule this establishes: a compound that raises nitric oxide is not a fat-release agent, however good it is for blood flow. The two effects are separable and they point in opposite directions. The field itself is cautious: 'the effect of nitric oxide appears complex and is not fully understood'. PMID 10323597
It increases Fat-cell formation↓.
Two different enzymes make the same messenger, and in fat they do opposite things. This is the most counter-intuitive finding on this MAP and it overturns the obvious assumption. The messenger made at the heart-peptide receptor releases fat. The same messenger made by the nitric-oxide enzyme does the reverse. Measured in living people, not in cells: 'the NO synthase inhibitor, L-NMMA, but not the biologically inactive enantiomer, increased glycerol levels in the microdialysates without causing a change of local blood flow... Nitric oxide gas as well as the NO donor, NITROGLYCERINE, reduced glycerol release from isolated adipocytes' (PMID 10323597 — a nitric oxide-mediated mechanism regulates lipolysis in human adipose tissue in vivo (microdialysis)). ⇒ blocking nitric oxide raises fat release. Supplying it lowers fat release. And the blood-flow explanation is ruled out in the same experiment. It also favors fat cell formation: 'nitric oxide and downstream second messenger cGMP and cAMP enhance adipogenesis in primary human preadipocytes' (Cytotherapy 2010 — Nitric oxide and downstream second messenger cGMP and cAMP enhance adipogenesis in primary human preadipocytes). The practical rule this establishes: a compound that raises nitric oxide is not a fat-release agent, however good it is for blood flow. The two effects are separable and they point in opposite directions. The field itself is cautious: 'the effect of nitric oxide appears complex and is not fully understood'. PMID 10323597
Blends that modulate it
Each blend page names this pathway and carries the study behind its claim.
See it on the map
Open the causal map to follow this pathway upstream and downstream, arrow by arrow, each with its study.