GIP

All articles tagged with “GIP”

Protocols

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

PeptidesPeptide

Tirzepatide

The first dual-action incretin that outpaces single-agonist therapy across weight, glucose, heart failure, and sleep apnoea, while forcing medicine to reckon with the musculoskeletal cost of rapid metabolic transformation.

Tirzepatide is an imbalanced dual GIP/GLP-1 receptor agonist achieving 15-22.5% body weight reduction, HbA1c cuts of up to 2.6%, FDA approval for sleep apnoea, and a 38% reduction in heart failure events. Its biased agonism at the GLP-1 receptor avoids receptor desensitisation, but rapid weight loss raises real concerns about bone density and lean mass.

tirzepatide

Protocols

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

PeptidesPeptide

Tirzepatide

The first dual-action incretin that outpaces single-agonist therapy across weight, glucose, heart failure, and sleep apnoea, while forcing medicine to reckon with the musculoskeletal cost of rapid metabolic transformation.

Tirzepatide is an imbalanced dual GIP/GLP-1 receptor agonist achieving 15-22.5% body weight reduction, HbA1c cuts of up to 2.6%, FDA approval for sleep apnoea, and a 38% reduction in heart failure events. Its biased agonism at the GLP-1 receptor avoids receptor desensitisation, but rapid weight loss raises real concerns about bone density and lean mass.

tirzepatide

gip

glp-1

mounjaro

zepbound

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