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Posted on Sunday September 28, 2025 in Metabolic Health
An article written by Dr Edward Leatham, Consultant Cardiologist
Tags: VAT, GLP-1, Inflammation, Diet, CKD, search website using Tags to find related stories.
In a related article, I explored how your mitochondria — the cellular “power stations” that produce energy — can become overwhelmed by surplus fuel, especially in the form of glucose.
When mitochondria process more fuel than your body needs, they begin to leak free radicals, triggering inflammation and long-term damage.
But under normal circumstances, how does excess energy get managed, when it can’t be immediately used?
It’s stored as fat — and the location of that fat matters far more than most people realise.
Today, we are looking at visceral fat — what it is, why it’s so dangerous, and how it’s part of a vicious metabolic feedback loop involving glucose overload, inflammation, and declining muscle function.
Visceral adipose tissue — or VAT — is the fat stored deep inside your abdomen, wrapped around your organs: liver, intestines, pancreas, kidneys. In small quantities it is protective by cushioning the vital organs
When present in excess, visceral adipose tissue is different from subcutaneous fat (the soft, pinchable kind under your skin). VAT is hidden, but far more metabolically active — and problematic.
VAT acts like a rogue endocrine organ. It doesn’t just store energy. It releases inflammatory molecules, interferes with insulin sensitivity, and is strongly linked to:
As VAT grows it starts to push your abdomen out and your waist circumference grows. In fact, due to the negative effects of visceral fat, your waist-to-height ratio is now recognised as a more powerful predictor of metabolic risk than BMI.
Every time you eat a high-carbohydrate meal — especially one low in fibre and protein — your blood glucose rises. If your muscles are active and insulin is functioning well, that glucose is taken up and burned for energy. In people with a carbohydrate sensitive phenotype it appears the glucose clearance systems are not sufficient to clear the surplus so you can see short periods of high glucose in the circulation (spikes) as an early sign of the problem.
However it is clear whether you have csp or not , if your muscle mass is low (as in age-related sarcopenia), or you are sedentary, or your mitochondria are already saturated with fuel, the insulin triggered by the rise in glucose will signal storage processing, initially short term glycogen in muscle and liver then converting to Triglycerides for long term storage (your battery).
As we explained in a related blog on mitochondria, this is like solar panels producing too much energy for a full battery — the system overheats, and damage follows.
In the body, this excess energy is redirected into fat storage.
At first, it accumulates in subcutaneous tissue. But over time — especially in genetically susceptible people — fat begins to collect viscerally, inside the abdominal cavity.
Not everyone responds the same way to surplus calories — particularly carbohydrates.
In clinic, we see patients with “normal” weight but large waist circumferences, significant VAT on CT scans, and signs of early insulin resistance or inflammation — all driven by a mismatch between intake, clearance, and demand.
Here’s where things get really dangerous.
As VAT expands, it starts doing much more than storing fat:
This creates a vicious cycle:
More VAT → more FFA + inflammation → insulin resistance → reduced glucose disposal by muscle → more glucose in bloodstream → more fat storage (especially visceral)
Meanwhile, ageing reduces muscle mass (sarcopenia), further decreasing the body’s ability to absorb and use glucose efficiently. Mitochondrial function declines, especially in muscle and liver, compounding the problem.
VAT is more dangerous than subcutaneous fat because it is:
VAT contributes to the development of:
And it does so not just by being “extra fat,” but by actively sabotaging mitochondrial and muscle function.
To reverse this cycle, we need to:
The earlier this cycle is identified, the more reversible it is.
| Factor | Effect |
|---|---|
| Excess glucose | Overloads mitochondria → ROS → inflammation |
| Ageing + inactivity | Muscle loss → reduced glucose clearance |
| VAT growth | Releases FFA + cytokines → worsens insulin resistance |
| Inflammation | Further impairs mitochondrial function |
| Result | Accelerated metabolic dysfunction and ageing |
VAT is not just a by-product of weight gain — it is a key player in metabolic disease.
Its expansion is often the body’s final attempt to store energy that cannot be used or burned. But once it reaches a certain threshold, VAT becomes inflammatory, insulin-resistant, and metabolically toxic.
To prevent this, we must understand how modern life — constant food intake, refined carbohydrates, sedentary routines — overwhelms the mitochondria, depletes muscle, and promotes visceral fat storage.
When you see VAT not just as fat, but as a marker of mitochondrial overload, everything changes.
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