41. Basic characteristics and forms of diabetes mellitus syndrome

Page created on March 24, 2019. Last updated on May 18, 2019 at 20:26

I don’t know why the department calls it «diabetes mellitus syndrome». Nobody else does that. A syndrome is a constellation of symptoms that don’t have an identifiable cause, a definition diabetes definitely doesn’t fit. Diabetes mellitus is a group of diseases, not a syndrome.


Diabetes mellitus (DM) is a group of metabolic diseases that are characterised by chronic hyperglycaemia due to absolute or relative insulin deficiency. The decreased insulin effect causes insulin-dependent tissues to have smaller capacity to take up glucose.

The word diabetes refers to “excessive urine”, and mellitus means “sweet”. This refers to two of the most characteristic symptoms of DM, polyuria and glycosuria. The high plasma glucose level overloads the reabsorption capacity of the proximal tubules, causing some glucose to remain in the filtrate. This glucose is osmotically active, causing osmotic diuresis and polyuria.

As glucose is osmotically active will hyperglycaemia cause high osmotic pressure in the body. This, along with polyuria-induced hypovolaemia stimulates thirst, causing characteristic polydipsia.

As the insulin-dependent tissues can’t utilize glucose they must utilize other energy sources like fats and proteins. This causes the body weight to decrease. Glucose-loss through the urine contributes to the weight loss.

The more serious complications of diabetes are described in topic 45-47.

There are many types of diabetes mellitus. They’re grouped into four categories by the WHO:

  1. Diabetes mellitus type 1 – insulin-dependent DM
    • Type 1A – autoimmune type
    • Type 1B – Idiopathic type
  2. Diabetes mellitus type 2 – insulin-independent DM
  3. Other types of DM
    • MODY – maturity onset diabetes of the young
    • Diseases of the exocrine pancreas – pancreoprivic diabetes
    • Endocrinopathies
    • Drug-induces diabetes
  4. Gestational diabetes
Diabetes mellitus type 1 and 2

Also called 1DM or T1D and 2DM or T2D, these types are the most common.

Type 1 diabetes is (most commonly) the result of an autoimmune response that causes the destruction of the insulin-producing β-cells. This causes an absolute insulin deficiency. Both type 1A and 1B exist. 1A is the classical type, where autoantibodies are present. 1B is an idiopathic type, where no autoantibodies can be found.

Type 2 diabetes is much more common than type 1. It has a strong genetic component as well as significant association with obesity and sedentary lifestyles. It is characterised by insulin resistance, where insulin-dependent tissues like muscle and adipose tissue have insufficient response to insulin. This called relative insulin deficiency.

Their differences are summed up in the table below:

DM type 1 DM type 2
Incidence 10 % of all DM cases 90% of all DM cases
Inheritance Associated with certain types of HLA Independent of HLA
Concordance 40% 80 – 90%
Relation to metabolic syndrome None High
Evoking factor Infection or toxin No evoking factor
Time of development Before 25 years of age Mostly after 30 years of age
Initiation Fast Gradual
Blood glucose stability Unstable, depends on diet Stable at higher levels
Insulin need Obligatory First no, in later cases yes
β-cells Almost or totally lost Initially normal, later abnormal
Ketoacidosis Frequent Not typicall
Insulin resistance None Characteristic, severe

Concordance refers to how likely it is for one identical twin to get the disease when the other twin already has it. A concordance of 90% means that 90% of people who have an identical twin with the disease will develop the disease themselves. This shows that there is a significant genetic component to the development of 2DM.

1DM and 2DM are chronic, progressive diseases that warrant a comprehensive treatment approach to minimize potential complications. The main aim of the treatment is to keep the long-term average blood glucose (HbA1c) below 7%.

Other types of DM

The most important type of DM here is MODY, which stands for maturity onset diabetes of the young. As the name suggests it manifests in people younger than 25. This form is autosomal dominant and is not associated with obesity or autoantibodies.

Any disease that damages the pancreas as a whole can destroy the Langerhans islets and cause pancreoprivic diabetes. This can occur in haemochromatosis, cystic fibrosis or chronic pancreatitis, among others.

Because diabetes is defined as a chronic hyperglycaemia can overproduction of any insulin-antagonist hormone cause a form of diabetes. This includes cortisol treatment, Cushing disease, acromegaly and others.

Gestational DM

In ca 5% of all pregnancies will an otherwise non-diabetic mother develop impaired glucose tolerance. This occurs mostly during the second and third trimesters due to hormonal changes. The risk factor for developing gestational DM are the same for developing 2DM. In two thirds of the cases it ceases after delivery. In the remaining third 2DM develops. Mothers who have had gestational DM during previous pregnancies have higher risk of developing it again.

4 thoughts on “41. Basic characteristics and forms of diabetes mellitus syndrome”

    1. That’s a good question. The value has been chosen by various authorities on diabetes and health. While it does seem weird at first glance that values between 6.4 and 7% are considered okay, I’m sure there are some reasons behind it. The only one I can think of is to minimize the risk of hypoglycaemia, if not only that maintaining an HBA1c below 7% requires more effort and compliance from the patient than the benefits it brings. It’s probably better for the patient to have an achievable therapeutic goal rather than one that seems unachievable.
      You can read more about it here: https://blog.virtahealth.com/new-hba1c-targets-type-2-diabetes/ and probably many other places on the Internet.

    1. Prolactinoma is mentioned in the book as a potential cause of other DM, but I can’t find any support for that online. I’ll remove it from the topic as it’s probably not important anyway.

      My theory is that it could have something to do with the structural similarity of prolactin with GH.

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