The Growth Signaling Link Between Fat Gain, PCOS, Fibroids, and Fatty Liver

If you’re doing everything right but belly fat continues to accumulate , the issue is often upstream growth signaling. This often has to do with insulin. Here’s what I mean.

Insulin and IGF-1 activate pathways that regulate fat gain, cell growth, and glucose metabolism.

When these pathways remain chronically stimulated, multiple tissues respond:

• More fat gets stored
• The liver increases fat production
• A1C rises
• Ovarian androgen output increases (PCOS)
• Smooth muscle cells in the uterus receive more growth signals (fibroids)

Each condition presents differently. The metabolic environment overlaps.

Persistent hyperinsulinemia suppresses hormone sensitive lipase, preventing fat release at the enzymatic level.

Two days of training reduces insulin temporarily.

Five days of consistent resistance work lowers baseline insulin.

When baseline insulin falls:

Fat burning resumes.
mTOR signaling amplifies, which increases muscle growth.
Hepatic fat production slows.

Fat loss is often an early measurable signal that the growth dominant environment is correcting.

It is visible evidence of systemic metabolic improvement.

If you suspect growth signaling is keeping fat locked, schedule a session.

I will help you evaluate whether insulin dynamics, training structure, or glucose variability are maintaining a storage dominant state.