- Social Impact of Diabetes Mellitus
- Diabetic Complications
- Biochemical mechanism of the development of diabetic complications
Social Impact of Diabetes Mellitus
- 1.4 million (3%) of the U.K. population are diabetic; a further 3% undiagnosed diabetics. 6-8% of USA population are diabetics.
- 10% have Type 1 diabetes mellitus; 90% have Type 2 diabetes mellitus.
- Both Type 1 and Type 2 diabetes mellitus have increased risk of heart disease, stroke, retinopathy, nephropathy and peripheral neuropathy.
A further 10% of the population has impaired glucose tolerance (IGT) with increased risk of developing Type 2 diabetes mellitus and complications
Retinopathy, neuropathy, nephropathy, macrovascular disease - myocardial infarction, angina, stroke, cataract, embryopathy - also impotence and foot ulceration. All of these are known complications with diabetes.
Prevalence increases with duration of diabetes: after 20 years of diabetes, 87% of type 1 diabetic patients and 53% of type 2 diabetic patients have retinopathy - about a quarter of these have proliferative retinopathy. Diabetes is a major cause of blindness.
Apparent in 20% of diabetic patients. Sensory neuropathy - affecting feet and legs, sometimes also arms. Unpleasant sensations (tingling, burning, severe cramps, shooting pains; later, numbness). Amyopathy - severe pain and wasting in muscle of thighs and lower leg. Can also affect arms. Other focal neuropathies - carpal tunnel syndrome and cranial palsies.I/p>
Apparent in 20-25% of diabetic patients (45% of type 1 patients - half die from renal failure or associated vascular disease). Basement membrane and mesangium thickening, and glomerulosclerosis.
Diabetics suffer from an increased risk of coronary heart disease: 2-3 fold in men, 4-5 fold in women.
Increased rate of perinatal mortality (stillbirths, neonatal deaths) and embryo malformations: 5.6% in diabetic, 1.4% in non-diabetic women.
Biochemical mechanism of the development of diabetic complications
Associated with cells with insulin INDEPENDENT uptake of glucose by the GLUT1 glucose transporter – blood capillary endothelial cells and pericytes, lens fibre cells, peripheral neurones.
Intracellular hyperglycaemia leads to biochemical dysfunction – accumulation of triosephosphates and associated biochemical dysfunction.