Seven Ways To Combat Insulin Resistance with Type 1 Diabetes

Overview

This page explains the seven practical levers that most reliably improve insulin resistance in people with type 1 diabetes. It stacks interventions like a pyramid: lifestyle foundations first, then pharmacology where appropriate.

Insulin resistance in T1D is rarely “one thing”. It usually emerges from overlapping disturbances across muscle, liver, adipose tissue, gut hormone signalling, and brain insulin sensitivity. This page focuses on what tends to shift the system meaningfully in the real world.

Prefer audio? Listen to GNL Podcast Episode 14.

The detail

If you want a single organising principle: insulin resistance is usually improved most by (1) movement, (2) body fat reduction where appropriate, and (3) reducing glucotoxicity. Pharmacology can be powerful — but it works best when layered onto the foundations.

Below are the seven pillars. The art is choosing the smallest set that meaningfully shifts your trajectory.

1) Activity (aerobic + resistance + daily movement)

Physical activity improves insulin sensitivity through several mechanisms at once: increased glucose uptake (including non-insulin-mediated uptake), improved muscle insulin signalling, reduced intramuscular lipid burden (DAGs), improved hepatic insulin sensitivity, and improved appetite regulation via brain signalling.

Fasted exercise: Morning exercise performed at low circulating insulin levels may favour greater fat oxidation and often improves whole-day insulin sensitivity.
10–15 minutes after meals: reduces post-meal peaks and “supercharges” the circulating meal insulin, so less is required for the same effect.
Strength training 3–4×/week: increases muscle mass and glucose disposal capacity (huge leverage).
Aerobic training 3–5×/week: helps clear intramuscular lipid burden (DAGs) and improves hepatic control.
Daily movement: breaks sedentary time and keeps insulin action more predictable.
Activity snacking: small bursts of movement to reduce glucose and metabolic load without “a workout”.

Essential point: increasing activity often requires pre-planned insulin reductions. Otherwise, the “intervention” becomes a hypoglycaemia generator.

Resources:

2) Weight management (fat loss where appropriate)

Where excess body fat (especially visceral/ectopic fat) is present, fat loss can materially improve insulin sensitivity. Even 5–10% weight loss can be meaningful; 15–20% can be transformative for hepatic and muscle insulin resistance in many people.

The goal is fat loss with muscle preservation.

Protein: aim ~1.5–2.0 g/kg/day to support satiety and preserve lean mass.
Resistance training: At least 3–4×/week while losing weight.
Energy deficit: often ~500–1,000 kcal/day for ~0.5–1.0 kg/week loss (adjust to the individual).
Sleep and stress: Poor sleep / chronic stress makes fat loss harder.

3) Nutrition (reduce glucotoxicity, reduce “fat switch” inputs)

Nutrition influences insulin resistance through energy balance, glucose exposure (glucotoxicity), lipid exposure (lipotoxicity), and gut hormone signalling.

Limit liquid sugar / fructose-heavy inputs (a common lever on hepatic de novo lipogenesis). Listen to Attia #87 — Rick Johnson on fructose
Prioritise fibre-rich whole foods to slow absorption and improve satiety.
Watch for saturated fat load if delayed spikes and insulin resistance patterns are prominent.
CGM feedback loop: use CGM patterns to refine meals, not to chase perfection. See the CGM guide.
Pre-bolus (where appropriate): often ~15–20 minutes before meals for better matching (individualise for gastroparesis/AID etc.). See the Bolus guide.
Hypo treatment: prefer glucose-only options rather than mixed sugars that can stack unpredictably.

4) GLP-1 receptor agonists (semaglutide) and dual agonists (tirzepatide)

GLP-1–based therapies are a legitimate pillar for insulin resistance management when obesity and/or appetite dysregulation are part of the picture, even though most use in T1D is currently off-label in many systems.

Mechanistic reasons these may help in T1D (beyond weight loss): reduced glucagon output, reduced hepatic glucose output, improved satiety signalling, and slower gastric emptying (which can improve matching when handled carefully).

Safety first (T1D-specific)

Insulin requirements can fall quickly (often discussed around ~30% early on in practice) → without planned reductions, hypos are likely.
Slower gastric emptying can make bolus timing harder (especially off AID).
Muscle preservation matters during weight loss: pair with protein + resistance training.

Do not DIY this. Use a clinician and a protocol.

Resources:

GLP-1 FAQ
GLP-1 Podcast

5) SGLT-2 inhibitors

SGLT-2 inhibitors lower glucose by increasing urinary glucose excretion, reducing glucose toxicity, and (often) insulin requirements without directly increasing insulin.

Potential benefits: lower glucose exposure, less insulin required, sometimes improved variability.
Major risk in T1D: DKA (including euglycaemic DKA) if used without strict education and protocols.
Practical: hydration, ketone monitoring, sick-day rules, and clear stop rules are non-negotiable.

This is firmly “discuss with your team” territory.

6) Pioglitazone (PPAR-γ agonist)

Pioglitazone can improve insulin sensitivity partly by redistributing fat away from ectopic depots (liver/muscle) towards safer subcutaneous stores. It is often avoided because of “weight gain”, but the mechanism is more nuanced than that.

Potential upside: improved hepatic and muscle insulin signalling.
Trade-offs: fluid retention risk (and other contraindications), slower onset (weeks–months), and careful patient selection.
Best paired with resistance training and adequate protein to protect lean mass.

7) Metformin (mostly hepatic)

Metformin is often described as a general insulin sensitiser, but mechanistically, its clinically relevant effects are largely hepatic (liver). It reduces hepatic glucose output and can reduce glucose toxicity. It does not directly “fix” muscle insulin resistance.

Typical insulin-lowering effect in T1D is often modest (commonly cited around ~5% in practice summaries).
Still useful in a multi-lever approach because it is cheap and has a long safety record (with appropriate monitoring and contraindications respected).

Mechanism deep dive: Attia #337 — Ralph DeFronzo masterclass

Practical

Start with the foundations first. For most people, the fastest “ROI” comes from (1) movement, (2) fat loss where appropriate, and (3) reducing glucotoxicity. Add drugs only when the leverage is worth the monitoring burden and the risk profile.

If you increase activity: plan insulin reductions ahead of time to prevent hypos from becoming the limiting factor.
Limit saturated fat: favour fibre-rich foods and induce an energy deficit (500-1000 kcal/day). Small, consistent shifts can meaningfully reduce lipid-driven insulin resistance over time.
If you pursue fat loss: protect muscle (protein ~1.5–2.0 g/kg/day + resistance training 3–4×/week).
If considering GLP-1 / dual agonists: expect insulin needs can fall quickly (often ~30% early in practice) and bolus timing may need changes due to slower gastric emptying.
If considering SGLT-2 inhibitors: DKA risk is the price of entry. Ketone education, sick-day rules, hydration, and clear stop rules are non-negotiable.

Key idea: the goal is not to do everything. The goal is to choose the smallest set of levers that measurably reduces insulin dose requirements, improves predictability, and lowers glucose exposure over time.

Seven Ways to Combat Insulin Resistance with type 1 diabetes