Koveras
Member
- Joined
- Dec 17, 2015
- Messages
- 720
"In 1994 A.V. Sirotkin found that melatonin inhibits progesterone production but stimulates estrogen production, and it’s widely recognized that melatonin generally inhibits the thyroid hormones, creating an environment in which fertilization, implantation, and development of the embryo are not possible. This combination of high estrogen with low progesterone and low thyroid decreases the resistance of the organism, predisposing it to seizures and excitotoxic damage, and causing the thymus gland to atrophy." -Ray Peat, PhD
"Although melatonin sometimes antagonizes serotonin in a protective way, in itself it can lower body temperature and alertness, suppressing thyroid and progesterone. (Sirotkin, 1997)" -Ray Peat, PhD
Increased Melatonin Signaling Is a Risk Factor for Type 2 Diabetes
-rs10830963 is an eQTL in human islets conferring increased MTNR1B mRNA expression
-Melatonin inhibits cAMP rises in mouse islets and clonal insulin-secreting cells
-Melatonin blocks insulin release in mouse islets and clonal insulin-secreting cells
-Melatonin’s inhibition of insulin release is stronger in risk allele carriers
"Type 2 diabetes (T2D) is a global pandemic. Genome-wide association studies (GWASs) have identified >100 genetic variants associated with the disease, including a common variant in the melatonin receptor 1 b gene (MTNR1B). Here, we demonstrate increased MTNR1B expression in human islets from risk G-allele carriers, which likely leads to a reduction in insulin release, increasing T2D risk. Accordingly, in insulin-secreting cells, melatonin reduced cAMP levels, and MTNR1B overexpression exaggerated the inhibition of insulin release exerted by melatonin. Conversely, mice with a disruption of the receptor secreted more insulin. Melatonin treatment in a human recall-by-genotype study reduced insulin secretion and raised glucose levels more extensively in risk G-allele carriers. Thus, our data support a model where enhanced melatonin signaling in islets reduces insulin secretion, leading to hyperglycemia and greater future risk of T2D. The findings also imply that melatonin physiologically serves to inhibit nocturnal insulin release."
"Although melatonin sometimes antagonizes serotonin in a protective way, in itself it can lower body temperature and alertness, suppressing thyroid and progesterone. (Sirotkin, 1997)" -Ray Peat, PhD
Increased Melatonin Signaling Is a Risk Factor for Type 2 Diabetes
-rs10830963 is an eQTL in human islets conferring increased MTNR1B mRNA expression
-Melatonin inhibits cAMP rises in mouse islets and clonal insulin-secreting cells
-Melatonin blocks insulin release in mouse islets and clonal insulin-secreting cells
-Melatonin’s inhibition of insulin release is stronger in risk allele carriers
"Type 2 diabetes (T2D) is a global pandemic. Genome-wide association studies (GWASs) have identified >100 genetic variants associated with the disease, including a common variant in the melatonin receptor 1 b gene (MTNR1B). Here, we demonstrate increased MTNR1B expression in human islets from risk G-allele carriers, which likely leads to a reduction in insulin release, increasing T2D risk. Accordingly, in insulin-secreting cells, melatonin reduced cAMP levels, and MTNR1B overexpression exaggerated the inhibition of insulin release exerted by melatonin. Conversely, mice with a disruption of the receptor secreted more insulin. Melatonin treatment in a human recall-by-genotype study reduced insulin secretion and raised glucose levels more extensively in risk G-allele carriers. Thus, our data support a model where enhanced melatonin signaling in islets reduces insulin secretion, leading to hyperglycemia and greater future risk of T2D. The findings also imply that melatonin physiologically serves to inhibit nocturnal insulin release."