Weight, Dental Disease and the Other Things That Quietly Wreck Control

Almost any source of infection or inflammation in the body can blunt how well the tissues respond to insulin (Ridgway, 2015), so the same dose stops doing the same job and a comfortably-controlled pet starts to look under-dosed. The veterinary consensus names this plainly: a diabetic's responsiveness to insulin can be reduced by concurrent inflammatory, infectious, neoplastic or hormonal disorders, and the commonest concurrent problems are hyperadrenocorticism, urinary tract infection, dermatitis, otitis, acute pancreatitis, neoplasia and hypothyroidism (Behrend et al., 2018). Three of those seven, the urine infection, the skin and the ears, are exactly the everyday things this article is about.

That matters because the obvious-looking response, reaching for more insulin, is often the wrong first move. Factors other than true insulin resistance are the more common causes of poor control early on, so the teaching is to find the cause and treat it, then re-regulate around it, rather than chasing higher doses (Ridgway, 2015). There is a dose level at which your vet starts formally hunting for a hidden driver, but that work-up lives in its own guide, when the insulin just won't work. So please don't increase the dose yourself off a single high reading. Control is about trends, not one number, and the dangerous mistake is to keep climbing the dose when the real problem is something else.

Weight is the destabiliser you have the most direct control over, but I have to be precise, because it does genuinely different things in a cat and a dog, and almost every page online blurs the two.

In cats, fat is not innocent. Obesity is a real cause of insulin resistance and of feline diabetes: overweight cats are two to four times more likely to develop diabetes than ideal-weight cats, with roughly a 30% decline in insulin sensitivity for every kilogram of excess body weight (Clark & Hoenig, 2021), and one experimental study found about a 52% fall as cats became obese (Appleton et al., 2001). The hopeful flip side: getting that weight off normalises insulin sensitivity, can lower the dose, and improves the odds of control and even remission (Clark & Hoenig, 2021; Taylor et al., 2025). It pays to act early, because losing at least 2% of body weight in the first month of insulin treatment is one of the better predictors of remission, with one report describing roughly a fifteen-fold increase in the odds of coming off insulin (Taylor et al., 2025). For a fat diabetic cat, weight loss is one of the most powerful things you can do. The remission playbook is in giving your cat the best shot at remission, and diet as a control lever in diet as a lever.

In dogs, the story is honestly different. Obesity worsens insulin sensitivity and makes control harder, but it is not an established cause of canine diabetes the way it is in cats. Canine diabetes is largely immune-mediated and pancreas-related, and as the research bluntly notes, dogs are resistant to developing type-2 diabetes; the large UK primary-care data did not confirm obesity as a risk factor for the disease at all, concluding more research is needed to establish the link (Heeley et al., 2020). The fair summary is a specialist's: in dogs, obesity causes a reversible, usually fairly mild insulin resistance, readily overcome by adjusting the dose and by weight loss (Ridgway, 2015). So a healthy weight still helps a diabetic dog's control and general health, but don't let anyone sell it as the cause of the disease, or as a cure.

Either way, the safety rule is the part owners miss. Weight comes off slowly and under supervision, around 0.5 to 1% of body weight a week for a cat, aiming for a body condition score of 5 out of 9 (Taylor et al., 2025), and roughly 1 to 2% a week for an overweight dog (Behrend et al., 2018). Here is the crucial seam: losing weight lowers insulin need, so the dose that suited a heavier pet can become too much as the weight comes off. Reduce it with your vet as you go, with home monitoring, or your pet can tip into a hypo. One universal caveat: a thin diabetic should never be put on a slimming diet. The goal is to normalise weight, not strip it off a pet who hasn't got it to spare (Behrend et al., 2018). For context, pet obesity is rife in the UK, with vets estimating around 46% of dogs overweight or obese and most owners under-recognising it (PDSA PAW Report, 2023).

If weight is the lever owners know, dental disease is the one they almost never connect, and it's among the most satisfying to fix. Periodontal disease, the chronic infection and inflammation of the gums and tooth roots, is the commonest oral disease in dogs and cats and tends to be worse in diabetics. The mechanism is the same low-grade-inflammation story as everywhere else here: a mouth full of chronic infection pours inflammatory signals into the body that blunt insulin's effect, the same two-way loop long established in human diabetes.

What lifts this from theory to something I can point to is direct evidence in dogs. In a recent prospective case series of ten dogs with poorly-regulated diabetes and periodontal disease, treating the periodontal disease improved their markers of glycaemic control, measured by fructosamine, HbA1c and inflammatory markers before treatment and monthly for three months, with the effect most conspicuous in the dogs whose disease was most severe (Nivy et al., 2024; Schermerhorn, 2024).

Let me be honest about that study rather than oversell it: it was small, only ten dogs, ran just three months, and the dogs' day-to-day signs didn't obviously change even as the laboratory markers improved. So I wouldn't promise a dental transforms control. But a sore, infected mouth is a real and fixable destabiliser, treating it can genuinely help, and it's worth doing for your pet's comfort regardless. An annual dental check, plus the odd look for red gums, brown tartar or bad breath, is one of the easier wins here.

These infections can sit quietly in the background and nudge insulin need up without making your pet obviously ill.

A urinary tract infection is the classic one, and it's worth getting right because the old teaching overstated it. It's one of the recognised concurrent problems in diabetics (Behrend et al., 2018), even a simple one can activate stress hormones and produce insulin resistance (Ridgway, 2015), and they're often silent, which is exactly why they're worth ruling out when control slips. But the modern picture is more measured than "every diabetic has a UTI": in a study of 107 diabetic dogs, only 14% had a positive urine culture, and nearly three-quarters of those had no urinary signs at all, with E. coli the commonest organism by far (Nelson et al., 2023). So a hidden UTI can wreck control and is worth testing for when things drift, but the responsible approach is to culture when there are signs or an active sediment, not to put every diabetic on rolling antibiotics. Current guidance is not to blanket-screen, but to consider treating a symptomless infection in a diabetic when it's thought to be driving insulin resistance or ketones (Weese et al., 2019). Test if indicated, treat what's real.

Skin and ear infections work the same way. Dermatitis and otitis are two more of the commonly-named concurrent disorders (Behrend et al., 2018), and a persistent pyoderma or grumbling ear infection activates the same counter-regulatory hormones and inflammatory signals that raise insulin need (Ridgway, 2015). So an itchy patch of skin or a smelly ear isn't only a comfort problem: it can be holding your pet's control back, and clearing it up often lets the glucose settle again. There's a hypo seam here too. When a hidden infection finally clears, the dose that was keeping up with it can suddenly be too much, so as it resolves, watch for the signs of a low and keep your vet in the loop.

This is the destabiliser I most want you to carry away, because it's the one good intentions trip over. Glucocorticoids, steroids, are potent drivers of insulin resistance and high blood sugar, and that includes not just tablets and injections but topical preparations: steroid skin creams, ear drops and eye drops all count.

The evidence is concrete in both species. In cats, a cohort on high-dose prednisolone (at least 1.9 mg/kg/day for more than three weeks) saw 9.7% develop steroid-induced diabetes, the great majority within the first three months (Nerhagen et al., 2021), and reassuringly, cats who become diabetic on steroids are more likely to remit once the steroid is stopped (Taylor et al., 2025). In dogs, UK primary-care data make it vivid: dogs had roughly four times the odds of being diagnosed with diabetes if exposed to glucocorticoids in the six weeks beforehand (Heeley et al., 2023). The mechanism is that steroids tell the liver to pump out more glucose and stop the tissues taking it up properly (Heeley et al., 2023; Ridgway, 2015). The same effect comes from progestogen hormones, so an unspayed female's season is worth flagging too.

Here's the practical gold, because owners often don't realise that a cream for an itchy paw, an ear or eye drop, or a steroid jab for some unrelated problem can knock a diabetic's control sideways. Two rules. First, tell every vet, nurse and pharmacist your pet is diabetic, every time, so nobody reaches for a steroid without weighing it. Second, never stop or change a steroid abruptly yourself: they usually have to be tapered, and stopping suddenly can cause real harm. If your pet is on one and the diabetes is misbehaving, that's a conversation with your vet, not a kitchen-table decision.

Beyond the everyday stuff sit bigger, less common drivers your vet looks for next: Cushing's disease, acromegaly, an overactive thyroid, pancreatitis, and the full hormonal picture in an intact female. Those get their proper explanation in the concurrent diseases that fight your insulin. For now, just know that if the ordinary suspects are ruled out and control is still poor, that's where the trail leads.

Most of what wrecks a diabetic's control is catchable in ordinary care, long before it becomes a crisis. Weigh your pet regularly and learn to body-condition score them, using the same scales and log you already keep. Look in the mouth now and then, and don't skip the annual dental. Watch for the itch-and-smell of a skin or ear problem, and mention any new thirst, increased weeing or off-food spell promptly, because it could be a brewing infection, and an off-food, vomiting diabetic can occasionally tip towards the more serious emergency of ketoacidosis. And flag the diabetes at every appointment, so no one reaches for a steroid unawares.

The thread that ties it together is the trend. Logging weight, the recheck numbers and your pet's glucose in one place, such as the Glucose Companion, means drifting control shows up as a slow bend in the line well before it shows up as a sick pet, and the same record shows the glucose recovering once you've fixed the cause. The formal recheck rhythm and what fructosamine adds is in fructosamine and the vet rechecks.

So if your pet's control has slipped, please don't assume you're failing at the injections. The far likelier story is one of these ordinary, fixable things, and the productive next step isn't a bigger dose, it's a careful look for the reason, with your vet, starting with the boring suspects first. That's the most hopeful thing about this stage: the commonest things that wreck control are also the ones you can do something about.