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Weight management and diabetes mellitus

LIBBY SHERIDAN reviews the links between the obesity and diabetes in dogs and cats and recent work on possible mechanisms

OBESITY is now recognised as a
major welfare issue in dogs and
cats, with an estimated 40% of our
nation’s pets now affected.

Its association with certain diseases
is well recognised. Both
hypothyroidism and
hyperadrenocorticism can predispose to obesity
(although the
percentage of obese
patients presenting
with such underlying
disease is very small,
possibly less than 1%).

By turn, obese
pets are at a higher
risk of respiratory
disease, urolith
formation and urinary
disease, mobility
problems resulting
from excessive load-
bearing on joints, and
poor coat and skin
disease from an
inability to groom
properly. An effect on
life-span has also been noted, with a
group of dogs fed an energy-restricted
diet living almost two years longer
than a moderately overweight group
which were fed ad lib.

Obesity and diabetes

A link with diabetes mellitus in both
dogs and cats is also well recognised.

In cats, obesity is a known risk
factor for the development of the
disease (increasing the risk by four-
fold), and obesity features strongly in
the growing number of diabetic cats.

In dogs, obesity has also been
reported to predispose to the disease
and to exacerbate its effects.

Many cats (up to 70% of newly
diagnosed cases) have “type II”
diabetes, although most will need
exogenous insulin in their
management. In some, the
pathogenesis seems to be one of
chronic insulin resistance, with obesity
leading to down-regulation of insulin

The body perceives this as a
relative lack of insulin (as the glucose
isn’t taken up by muscle and adipose
cells) and so more insulin is produced.
This then leads to chronic
hyperinsulinaemia, continuing
hyperglycaemia and “glucose toxicity”,
whereby beta cells eventually become
exhausted and the cat becomes
dependent on exogenous insulin.

Interestingly, though, this situation
appears reversible in some, and many
cats requiring insulin at presentation
may subsequently go into remission,
with the disease becoming sub-clinical
in a period of a few months.

All cats will benefit from early
diagnosis and good, aggressive
management with
insulin, a low-
carbohydrate, high-
protein diet and close
glucose monitoring. It
is thought that as
many as 60% of
diabetic cats (not all
of which are
overweight) may
benefit to the point
that they go into

management is an
important aspect of
this management for
obese patients, and many cats progressively
lose their dependence on insulin injections as they lose weight, either
requiring a reduced dose or in some,
none at all.

Feline expert Martha Cannon from
the Oxford Cat Clinic, however,
cautions against “too conservative”
treatment and relying on weight loss

“The evidence from studies is clear
– early, aggressive management with a
low-carb diet and an insulin regime
that provides good, round the clock
control of glucose works best for
getting cats into diabetic remission.

Weight loss will be an important
part of overall management but
people shouldn’t rely on it alone to
turn things round, otherwise by the
time they get the weight off safely they
may have allowed the diabetic state to
run on too long to get remission.”

Remission, though, may not be
permanent and the dependency on
insulin can come and go, as resistance
and beta cell function waxes and
wanes, or other factors come into play,
such as the regaining of weight or
introduction of drugs such as
corticosteroids or progestogens.

It is thought that for every
kilogram increase in body weight, there
is an associated 30% decrease in
insulin sensitivity. Furthermore, some
cats appear susceptible to developing
diabetes with weight gain, with an
inherent predisposition to glucose
intolerance. It may also be that certain
cats are unable to adapt to the
sustained need for hypersecretion of
insulin, caused by insulin resistance,
and as adaptive mechanisms fail, this
leads to clinical diabetes and the need
for exogenous insulin.

With dogs, our understanding of the
disease has also changed in recent years.
Once thought to present with “type I”
disease as a result of autoimmune
destruction of the beta cells in the pancreas,
diabetes in dogs is now
recognised to be
multifactorial and
occurs as a result of
several possible
pathological pathways,
leading to the same
clinical presentation.

In some dogs, a
similar process of
insulin resistance and
islet exhaustion may be
the culprit, whilst in others a chronic
destructive process such as pancreatitis
or autoimmunity (with possible breed-
predisposition) may be underlying.

Endocrine link

Work in recent years has started to
unravel possible mechanisms by which
obesity and diabetes mellitus could be

Our previously held assumption
that adipose tissue is an inert
substance has been challenged with the
finding that canine adipocytes are far
from quiescent. Rather, white adipose
tissue is now recognised to be an
active endocrine substance, secreting
peptide factors and cytokines, known
as “adipokines”.

These adipokines include those
substances with endocrine effects such
as leptin and adiponectin and others
with inflammatory effects such as
tumour necrosis factor alpha (TNFá) and interleukin-6.
These inflammatory proteins

increase as the weight of fat tissue
rises, with obesity now being
recognised as inducing a chronic
inflammatory state.

In cats, adiponectin stimulates fatty
acid oxidation and glucose uptake and
increases insulin sensitivity in muscle.
Plasma levels are low in obese cats, but
normalise with weight loss. In lean
cats, leptin decreases food intake and
increases energy expenditure.

Obese cats have also been shown
to have increased levels of leptin, but
appear resistant to its effects. Again,
levels appear to normalise with weight

“At risk” cats

Catching susceptible cats at an early,
pre-clinical stage is a clear incentive.
Some experts advocate regular monitoring of “at risk”
patients, with checking
of weight and body
condition score to pick
up trends, along with
urine monitoring.

Factors affecting
risk include:

  • age 7-10 years;
  • male neutered cats;
  • Burmese breed ( this has recently been shown to be a risk factor in UK cats, as well as Australian);
  • indoor, sedentary cats;
  • obese cats over 5kg in weight;
  • cats receiving corticosteroids or
    progestogen treatment.

Future promise

Human assays of proinsulin, which is
secreted along with insulin by beta
cells, have shown abnormalities in
obese and diabetic patients.

This knowledge has led to the
development of an assay for proinsulin
in cats, which holds promise in
identifying early pre-clinical states.

Researchers found that changes in
proinsulin secretion in some obese cats
were also observed in lean and obese
humans who went on to develop type
II diabetes. Research is ongoing but
may hold some key early diagnostic
advantages for the future.

  • References available on request from
    the author.

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