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💊 PIOGLITAZONE — THE INSULIN SENSITISER THAT DOES MORE THAN LOWER GLUCOSE!

Pioglitazone isn’t one of the newer diabetes medications — in fact, it’s quite an old one, but that doesn’t mean there’s nothing interesting about it!

In my experience, it’s rarely used, but it’s still included in the NICE NG28 updated 2026 guidance. So I think it’s a drug worth understanding!

It works in quite a different way from some of the other medications we use in type 2 diabetes.

🔑 Let’s go back to the lock and key…

Insulin is the key and the cells are the locks.

With insulin resistance, the locks aren’t responding properly. The pancreas may initially work harder by producing more insulin, but the body’s tissues aren’t responding as well to the insulin that’s already there.

Pioglitazone helps make those locks on the cells more responsive to insulin.

But there’s another really interesting part of the story…

🧈 It changes how fat is handled.

When someone is insulin resistant, fat tissue can release more fatty acids into the circulation. Some of those fatty acids end up in the liver, contributing to liver fat and further metabolic dysfunction.

Pioglitazone improves insulin sensitivity in fat tissue and can reduce this fatty-acid spillover — meaning it can reduce liver fat too.

So it isn’t simply:
“Take pioglitazone → lower the glucose.”

There’s a much bigger metabolic story going on.

⏳ BUT… it isn’t an instant fix.

Pioglitazone works gradually, so we shouldn’t expect an immediate change. Response and tolerability should be reviewed over time.

And, as always with diabetes medication:

The right drug for the right person matters. ❤️

Pioglitazone can cause fluid retention and weight gain, and is also associated with an increased risk of heart failure and fractures.

There are also important contraindications and precautions — which is why the person, their circumstances and their other medicines all need to be considered.

That’s why I really like my phrase:

1️⃣ Useful drug
2️⃣ For the RIGHT person
3️⃣ In the RIGHT circumstances

As I always say, diabetes care isn’t just about chasing the HbA1c down.

It’s about understanding WHY we’re choosing a treatment and whether it is right for the person sitting in front of us.

🔑 Pioglitazone doesn’t make more insulin keys.

It helps the locks respond better — and can reduce fatty-acid spillover to the liver too.

What do you think?

Did you know about the liver-fat effect of pioglitazone? 👇

Educational information only. This post isn’t a substitute for individual clinical assessment or prescribing guidance. Always refer to current guidance and the individual person’s circumstances.

Updating my previous posts - this time How does Gliclazide work? 💊

Gliclazide is a sulfonylurea — and unlike some of our newer diabetes therapies, its main action is to encourage the pancreas to release more insulin.

In simple terms, it stimulates the pancreatic beta cells to release insulin… or, for those who remember my slightly less professional explanation: “Spank the panc!” 😂

That extra insulin helps lower blood glucose — but it also explains the key downside of gliclazide: hypoglycaemia.

💡 More insulin = more hypo awareness needed.

The risk of hypoglycaemia increases when there is a mismatch between insulin, food and activity — for example, if meals are skipped or delayed, carbohydrate intake is significantly reduced, activity increases, or alcohol is involved.

There are a few other important things to remember:

🩸 Blood glucose monitoring isn’t routinely required for everyone taking gliclazide, but it may be appropriate in particular circumstances, including suspected/recurrent hypos or where hypoglycaemia risk has implications for driving or operating machinery.

🍽️ Take gliclazide as prescribed and according to the formulation — some preparations are taken shortly before a meal, while modified-release preparations have their own specific instructions. Regular meals remain important.

⚖️ Weight gain can occur with sulfonylureas.

🦽 Frailty matters — hypoglycaemia can increase the risk of falls, so treatment needs to be individualised.

And, as always, we’re not just treating a blood glucose number. Think about the person in front of you — their eating pattern, activity, renal function, other medicines, circumstances and individual treatment goals.

The key message?

Gliclazide stimulates insulin release → blood glucose falls → but hypoglycaemia can occur.

Know the risk. Recognise the symptoms. Know what to do. ❤️

Based on NICE NG28, updated February 2026.

🧓💜 Diabetes, frailty & deprescribing — treat the person, not the HbA1c

When someone living with Type 2 diabetes becomes frail, the question shouldn’t simply be:

“What’s their HbA1c?”

It should be:

“How is this person doing, and what matters to them?”

Frailty changes the balance between the benefits and burdens of diabetes treatment. As frailty increases, our focus often needs to shift from long-term risk reduction towards avoiding hypoglycaemia, reducing treatment burden, maintaining independence and improving quality of life.

And remember — deprescribing doesn’t mean abandoning diabetes care. 💜

For someone who is moderately or severely frail, QOF uses ≤75 mmol/mol as the threshold for its diabetes indicator. This is more relaxed than the indicator for people without moderate/severe frailty, but it should not be interpreted as “75 is the target for every frail person.” HbA1c targets should still be individualised.

For me, one of the most important questions is:

“How does their blood glucose make them feel?”

If someone is persistently hyperglycaemic and experiencing thirst, polyuria, nocturia, dehydration, fatigue or other symptoms of osmotic diuresis, simply accepting a high HbA1c because they are frail may not be the most person-centred approach.

Equally, if they are asymptomatic, treatment is burdensome, appetite is poor, falls are occurring or hypoglycaemia is becoming a concern, less may genuinely be more.

The 2026 NICE NG28 update reflects this beautifully — for people with frailty who need additional treatment, the emphasis is on managing hyperglycaemia symptoms and individualised glycaemic targets, while considering the increased risk of hypoglycaemia and falls associated with sulfonylureas and insulin.

So before we add another tablet or increase insulin, perhaps ask:

💜 What is the benefit for this person?
💜 What is the treatment burden?
💜 Are they having hypo symptoms or osmotic symptoms?
💜 What matters most to them?
💜 Can we simplify rather than intensify?
💜 Could we safely deprescribe?

Frailer does not = no treatment.

It means individualised treatment, fewer harms, less burden and more focus on the person sitting in front of us.

Because ultimately…

Treat the person, not the HbA1c. 💜💚💙

GLIPTINS (DPP-4 INHIBITORS) — HOW DO THEY WORK?

I’m continuing my “How do Type 2 diabetes medications work?” series, and this time we’re looking at the gliptins — or DPP-4 inhibitors.

You’ll probably be very familiar with these medications in primary care, but it’s always useful to go back to the physiology and remind ourselves what they’re actually doing!

🧠 The simple version:

1: When we eat, our gut releases incretin hormones, including GLP-1.

2: Normally, the enzyme DPP-4 quickly breaks GLP-1 down.

3: Gliptins inhibit DPP-4 → so the person’s own GLP-1 remains active for longer.

That increased GLP-1 activity helps to:

1: ⬆️ Increase insulin release when glucose is elevated
2: ⬇️ Reduce glucagon release
3: ⬇️ Lower blood glucose

Because the effect is glucose dependent, gliptins have a relatively low risk of hypoglycaemia when used alone.

They are also generally weight neutral and are taken orally, although dosing varies between individual gliptins and some require dose adjustment with reduced kidney function.

⚠️ Two important practice points

1️⃣ Pancreatitis

There is a rare risk of acute pancreatitis with DPP-4 inhibitors.

If someone taking a gliptin develops persistent, severe abdominal pain, particularly if it radiates to the back and may be accompanied by nausea or vomiting, think pancreatitis.

👉 If pancreatitis is suspected, discontinue the DPP-4 inhibitor.

2️⃣ Gliptins + GLP-1 RA/tirzepatide

This is particularly important with the 2026 update to NICE NG28.

A DPP-4 inhibitor should not be prescribed alongside a GLP-1 receptor agonist or tirzepatide.

They work along the same GLP-1 pathway, so there is no additional benefit from combining them.

👉 Starting a GLP-1 RA or tirzepatide? STOP the gliptin first.

The gliptins may not get as much attention these days with all the newer therapies available, but they still have a place in Type 2 diabetes management — and understanding why and when we use them is just as important as knowing their names.

Sitagliptin (is the most cost effective - as off patent) • Linagliptin • Alogliptin . Vildagliptin • Saxagliptin

As always, the medication choice should be based on the individual’s clinical circumstances, comorbidities, kidney function, frailty, treatment goals and their preferences — not simply on their HbA1c.

Hope you find the infographic useful for your next diabetes review! 💜💚💙

Following up on a comment in my recent post, I’ve been thinking about SGLT2 inhibitors in the very old person…

We quite rightly talk about the renal and cardiovascular benefits of SGLT2 inhibitors, and NICE NG28 (updated February 2026) now recommends their use in appropriate people with Type 2 diabetes and CKD, including at eGFR 20–30 ml/min/1.73m².

But what happens when the person in front of you is 85, 90… or even 94?

Does age itself mean we shouldn’t prescribe?

I don’t think it’s that simple.

The 2026 ADA Standards of Care recognise that older adults can gain similar or greater benefits from SGLT2 inhibitors than younger people, but also emphasise careful selection because older people are more vulnerable to volume depletion and those who are frail or prone to orthostatic hypotension need particular caution.

So perhaps the question shouldn’t be:

“Is this person too old for an SGLT2?”Instead, we need to ask:

“Is the likely benefit greater than the treatment burden and risk?”

For me, that means thinking about:

🔹 Frailty and functional status
🔹 Hydration and oral intake
🔹 Falls and postural hypotension
🔹 Urinary symptoms and ge***al infections
🔹 Comorbidities and polypharmacy
🔹 Goals of care and life expectancy
🔹 The person’s ability to manage the treatment — and the support available to them

And there is another important consideration…

Very old and frail people are underrepresented in clinical trials.

So while we have good evidence for SGLT2 benefits in older adults overall, the evidence becomes much less robust when we’re talking about the very old, frail and multi-morbid person.

That doesn’t mean don’t prescribe.

It means don’t prescribe by age alone — and don’t prescribe by algorithm alone.

Individualise. Discuss. Review.

I’d be really interested to hear how others approach SGLT2 prescribing in the very old or frail person. 💙💜💚

Coincidentally, there’s a good article on the topic of SGLT2i’s and ketoacidosis risk in this edition of Diabetes and Primary care. See link:

Case report: Diabetic ketoacidosis – a rare but serious side-effect of SGLT2 inhibitors - DiabetesontheNet Stef (a pseudonym) was a 53-year-old lady with a 6-year history of type 2 diabetes.

This is the link to the Diabetes Care and Management Foundation Course I designed and developed and keep updated on behalf of Rotherham Respiratory. It is ideal for any healthcare professional starting to work with / review people living with diabetes.
https://rotherhamrespiratory.com/pancreas-courses/foundation-course-in-diabetes-care-and-management-online/
It’s 15 hours online with 10 sections that can be completed over 2 months. There are video presentations included and access to me to ask questions via the platform. Please share with anyone who might be interested. Thanks 🙏

“Why don’t you start an SGLT2 inhibitor when HbA1c is above 80 mmol/mol?”

This was a question I was asked recently — and it’s a really good one because there isn’t actually a NICE rule saying that an HbA1c above 80 mmol/mol means you shouldn’t start an SGLT2 inhibitor.

The February 2026 NICE NG28 update has moved us towards earlier use of SGLT2 inhibitors for many people with type 2 diabetes, particularly because of their cardiovascular and renal benefits. So HbA1c >80 mmol/mol is not, in itself, a contraindication.

So why might I still pause and think carefully before starting one when the HbA1c is very high?

There are a few things I want to consider.

1: 🔹 Could there be significant insulin deficiency?

A very high HbA1c may indicate substantial β-cell dysfunction. I want to be confident that I’m not looking at someone with insulin-deficient diabetes, such as LADA or another form of diabetes where an SGLT2 inhibitor may increase DKA risk.

2: 🔹 What is the person’s DKA risk?

SGLT2 inhibitors can increase the risk of DKA, particularly when insulin availability is inadequate. Importantly, SGLT2-associated DKA can occur without the very high glucose levels we traditionally associate with DKA.

So I need to consider things such as previous DKA, illness, dehydration, very-low-carbohydrate/ketogenic diets and whether insulin is being reduced or stopped. NICE also emphasises the importance of sick-day guidance and avoiding initiation during illness or dehydration.

3: 🔹 What about tolerability?

SGLT2 inhibitors increase urinary glucose excretion and are associated particularly with ge***al mycotic infections such as thrush.

For someone who is already prone to recurrent infections, I want to discuss this before prescribing.

Why? Because a bad first experience can put someone off the whole class — and potentially mean we lose the opportunity to use a medication that could offer important long-term cardiorenal protection.

And this is where I think person-centred prescribing really matters.

I’m not thinking:

❌ “HbA1c >80 = don’t prescribe.”

I’m thinking:

✅ “HbA1c >80 = STOP • THINK • ASSESS.”

Is this the right person?
Is this the right time?
Could they be insulin deficient?
What is their DKA risk?
Are they likely to tolerate it?
Have they understood sick-day rules and ketone awareness?
And have we got the right follow-up in place?

So don’t just look at the HbA1c — look at the person.

That, for me, is the important message. 💙💜💚

Based on NICE NG28, updated February 2026. Clinical judgement and individual circumstances remain essential when prescribing.

💊 SGLT2 INHIBITORS — HOW DO THEY WORK?
A quick refresher on the SGLT2 inhibitor class and why these medicines have become so much more than glucose-lowering therapies.
🔬 How do they work?

SGLT2 is a transporter in the proximal renal tubule responsible for reabsorbing most filtered glucose back into the bloodstream.

SGLT2 inhibitors block this transporter, resulting in:
1: Reduced renal glucose reabsorption
2: Increased urinary glucose excretion
3: A reduction in blood glucose and HbA1c

And yes — quite simply, more glucose leaves the body in the urine/pee! 💧

❤️ But the important bit is what happens beyond glucose control…

SGLT2 inhibitors can provide important cardiorenal benefits, including reductions in heart failure hospitalisation and slowing progression of CKD in appropriate populations.

They can also produce:

1: Modest weight loss
2: A small reduction in blood pressure
3: Additional cardiovascular benefits in selected populations

Importantly, many of these benefits go beyond their effect on blood glucose.

💊 Examples of SGLT2 inhibitors include:

1: Dapagliflozin
2: Empagliflozin
3: Canagliflozin

⚠️ What do we need to remember?

The adverse effects and safety considerations are just as important as the benefits.

🔹 Ge***al mycotic infections are common
🔹 Increased urinary frequency can occur, particularly when starting treatment
🔹 Volume depletion can occur, particularly in people at greater risk of dehydration
🔹 SGLT2 inhibitors increase the risk of DKA — and DKA can occur without markedly elevated glucose

That last point is particularly important.

Sick-day guidance is essential. During significant illness, vomiting, dehydration or reduced food/fluid intake, SGLT2 inhibitors may need to be temporarily withheld according to local guidance.

So when considering an SGLT2 inhibitor, don’t just ask:

“What will it do to the HbA1c?”
Ask:
❤️ What are the person’s cardiovascular risks?
🫘 What is their kidney function and CKD risk?
⚖️ What other benefits might they gain?
⚠️ Are there any factors increasing their risk of adverse effects or DKA?

Because, as always, diabetes management is about the bigger picture — not just the HbA1c.

— Diabetes education that gives you the Keys to a Healthy Heart! 🔑❤️

💊 METFORMIN & VITAMIN B12 — SOMETHING WORTH KNOWING ABOUT

Metformin is an excellent medicine for Type 2 diabetes and is used by millions of people.

But did you know that metformin can reduce the absorption of vitamin B12, particularly with longer-term use?

Vitamin B12 deficiency can develop gradually, and the symptoms can be quite easy to put down to something else.

👀 Things to look out for include:

🔋 Unusual tiredness or fatigue
🧠 Poor concentration, memory problems or “brain fog”
⚡ Pins and needles, numbness or tingling
🚶‍♀️ Poor balance, unsteadiness or falls
😵 Dizziness or lightheadedness
👅 A sore, red or smooth tongue
🩸 Anaemia — although importantly, B12 deficiency can occur without anaemia
👁️ Blurred vision due to optic nerve problems — this is less common but important to recognise

So, should everyone taking metformin have their B12 checked?

Not routinely just because they take metformin.

NICE recommends being alert to B12 deficiency in people taking metformin, particularly when they develop symptoms or signs that could indicate deficiency.

The MHRA also advises considering periodic monitoring in people taking metformin who have additional risk factors for B12 deficiency.

Risk increases with factors such as longer-term metformin use, older age, low dietary B12 intake, previous B12 deficiency and conditions affecting B12 absorption.

💡 The important bit…

If you take metformin and develop symptoms that could be related to B12 deficiency, talk to your healthcare professional about whether your B12 level should be checked.

And if a deficiency is found, it can be treated — usually with vitamin B12 tablets or injections depending on the cause and severity.

❤️ Don’t stop your metformin because you’ve read this post!

This is about awareness, recognising symptoms and treating deficiency when it occurs.

As always, diabetes care is individual — speak to your healthcare professional if you’re concerned.

DiabEasyAs123 — making diabetes easier to understand. 🔑❤️