insulin sensitivity

All articles tagged with “insulin sensitivity”

Protocols

Blood Sugar Regulation

GLP-1 agonism is the headline. The full picture is three distinct peptide classes acting on glucose metabolism through three different mechanisms — and the honest protocol leads with the one that has actually passed regulatory scrutiny.

The peptide approach to blood sugar regulation splits into three distinct classes — incretin receptor agonists (GLP-1, dual GLP-1/GIP), mitochondrial-derived peptides (MOTS-c), and Khavinson bioregulators (Pankragen). Each sits on a different shelf of the evidence stack, each has a different risk profile, and the most common protocol error is treating them as interchangeable.

blood sugarmetabolic healthGLP-1semaglutidetirzepatide+5

Metabolic HealthOutcome

Insulin Sensitivity

Tirzepatide's insulin-sensitivity effect comes mostly from direct metabolic reprogramming, not weight loss. MOTS-c bypasses the insulin receptor entirely. The Khavinson bioregulators target β-cell regeneration via epigenetics. The three stories land at very different evidence grades — and the highest-impact decision in the whole class is sourcing.

Peptide therapy for insulin sensitivity now spans three distinct mechanistic classes: incretin agonists (GLP-1, tirzepatide, retatrutide) acting at the hormonal layer, mitochondrial-derived peptides (MOTS-c) acting at the cellular-energy layer via AMPK, and epigenetic bioregulators (Khavinson peptides, Pancragen) attempting to restore gene expression in β-cells. Weight loss explains only 13–21% of tirzepatide's HOMA-IR improvement — the rest is direct metabolic reprogramming. MOTS-c is an exercise mimetic in early trials. Bioregulators are a Russian-literature frontier awaiting Western replication. Sourcing is the biggest preventable harm in the whole class.

Protocols

Metabolic HealthOutcome

Blood Sugar Regulation

GLP-1 agonism is the headline. The full picture is three distinct peptide classes acting on glucose metabolism through three different mechanisms — and the honest protocol leads with the one that has actually passed regulatory scrutiny.

The peptide approach to blood sugar regulation splits into three distinct classes — incretin receptor agonists (GLP-1, dual GLP-1/GIP), mitochondrial-derived peptides (MOTS-c), and Khavinson bioregulators (Pankragen). Each sits on a different shelf of the evidence stack, each has a different risk profile, and the most common protocol error is treating them as interchangeable.

blood sugarmetabolic healthGLP-1semaglutidetirzepatide+5

Metabolic HealthOutcome

Insulin Sensitivity

Tirzepatide's insulin-sensitivity effect comes mostly from direct metabolic reprogramming, not weight loss. MOTS-c bypasses the insulin receptor entirely. The Khavinson bioregulators target β-cell regeneration via epigenetics. The three stories land at very different evidence grades — and the highest-impact decision in the whole class is sourcing.

Peptide therapy for insulin sensitivity now spans three distinct mechanistic classes: incretin agonists (GLP-1, tirzepatide, retatrutide) acting at the hormonal layer, mitochondrial-derived peptides (MOTS-c) acting at the cellular-energy layer via AMPK, and epigenetic bioregulators (Khavinson peptides, Pancragen) attempting to restore gene expression in β-cells. Weight loss explains only 13–21% of tirzepatide's HOMA-IR improvement — the rest is direct metabolic reprogramming. MOTS-c is an exercise mimetic in early trials. Bioregulators are a Russian-literature frontier awaiting Western replication. Sourcing is the biggest preventable harm in the whole class.

insulin sensitivitymetabolic healthtirzepatideGIPGLP-1+6