17. Pathology of obesity and diabetes

Last updated on December 7, 2018 at 13:45

Obesity

Obesity is defined as a state of increased body weight due to adipose tissue accumulation that can contribute to bad health effects. It’s an epidemiology that is rising for every year, and is related with diabetes, hypertension and physical inactivity.

How can you find out if someone is overweight or obese? The Body Mass Index (BMI) is said to be closely correlated with body fat and is a good way to find out if you for example are overweight. However, the BMI will not be the right method to choose if you have a lot of muscle, as muscle tissue weight is heavier than fat tissue weight.

Obesity can be divided into central and peripheral obesity.

Central obesity, also known as visceral obesity, is characterized by fat accumulating in the trunk and in the abdominal cavity around the organs and in the mesentery.

Peripheral obesity is just accumulation in subcutaneous tissue, as in the thighs, breasts and arms.

Of course, the central obesity will have a greater impact on the health because it involves the organs.

We might think that fat tissue is a stupid thing, but it’s actually important as it secretes leptin, a hormone that signals the brain to stop eating. However, some people develop leptin resistance, meaning that leptin loses its effect on the central nervous system so it no longer influences eating behaviour. You can read more about leptin here. Adipocytes also have the ability to convert testosterone into estrogen. This is the reason why obese men tend to get man boobs.

Why do we get obese? It’s a tricky question since genetics, environment and psychology may be factors, but it’s mostly a disorder of energy balance. The human body evolved to be in activity every day due to unpredictable lives where food was scarce and not readily available. The body is therefore not well adapted to environments where we have too much food. In the modern world, there is suddenly a lot of tasty food, but not enough activity.

Clinical consequences of obesity
  • Insulin resistance

Overnutrition makes the blood glucose level raise, so the insulin production increases to be able to lower the blood glucose. The insulin receptors will open up for glucose intake, making the cells store glucose as fat. This overnutrition makes the adipocytes full of fat and the muscles and liver full of sugar and glycogen, so they can’t handle any more glucose and shut down their insulin receptors. Pancreas try to produce more and more insulin to lower the sugar levels, but it will all result in hyperglycemia and hyperinsulinemia. High insulin levels prevent lipolysis and fat oxidation, but the patient is still hungry and tired. It becomes a viscous circle.

  • Type 2 diabetes
    • Especially central obesity
  • Cardiovascular disease
  • Hypertension
  • Cancer
    • High levels of insulin may increase levels of Insulin-like-growth-factor-1, (IGF-1), which stimulates growth and survival of cancerous cells.
  • Nonalcoholic steatosis
    • Fatty liver disease which can progress to fibrosis and cirrhosis without any alcohol involved. Read more about steatosis here and here.
  • Cholelithiasis
  • Hypoventilation syndrome – Pickwick syndrome
  • Joint diseases
  • Chronic inflammations
Diabetes mellitus

As many may have thought, including me, is that diabetes mellitus is a single disease, but it’s not. It’s a group of metabolic disorders sharing the underlying feature of hyperglycemia.

This hyperglycemia is often a result from defects in insulin secretion or insulin action, however, its most commonly due to both.

This chronic hyperglycemia is associated with damage of organs, especially the kidneys, eyes, nerves and blood vessels. Amputations of lower extremities, blindness in adulthood and end-stage renal disease is very often caused by untreated diabetes.

How do we know if anyone has diabetes mellitus? Since the insulin secretion or production is impaired, we can expect an undiagnosed person with diabetes to have high blood glucose levels:

  • A random blood glucose concentration of 11,1 mmol/L and higher, with classical symptoms as polydipsia (increased thirst), low energy and weight loss.
  • Fasting glucose concentration of 7 mmol/L or higher
  • Abnormal oral glucose tolerance rest (OGTT), where the glucose levels are higher than 11,1 mmol/L 2 hours after 75 g of glucose ingestion.

We divide diabetes mellitus into type 1 and type 2.

Diabetes type 1

This is an autoimmune disease where the body produces antibodies against the endogenous beta cell antigens. This leads to destruction of the β-cells in the pancreatic islets, so no insulin is produced. This type often develops in childhood, and progress with age.

Exogenous insulin is needed for survival.

Diabetes type 2

This type is a prototypical complex multifactorial disease where environment and diet play a major role, and genetic factors may also be involved.

There are two metabolic impairments that characterize type 2 diabetes:

  1. Tissues gets resistant to insulin.
  2. Beta cell dysfunction, making the secretion of insulin inadequate.

Amyloidosis of the Langerhans islets is very common in long-standing type 2 diabetes!

Complications of diabetes

Hyperglycaemia affects both the small and the large vessels, meaning we have both microvascular and macrovascular complications. Let’s take a closer look at what they are:

  • Microvascular
    • Retinopathy
    • Neuropathy
    • Diabetic nephropathy
  • Macrovascular

Hyperglycaemia accelerates atherosclerosis which affects the big and medium sized arteries. Atherosclerosis of the coronaries causing myocardial infarction is common, as well as stroke. The extremities, especially the lower, can become gangrenous because of peripheral artery disease due to atherosclerosis.


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16. General characterisation of amyloidosis. Physico-chemical, ultrastructural and histochemical nature of amyloid. Types of amyloid

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18. Causes of atrophy; general gross morphology and microscopical characteristics. Pathomechanism of atrophy. Hypoplasia, aplasia, agenesia. Osteoporosis.

2 thoughts on “17. Pathology of obesity and diabetes”

    1. Hi!
      It seems like the letter beta disappeared! Beta-cells are destructed in DM type 1. Thank you for letting me know 🙂 It is corrected now.

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