Diabetes Microvascular Complications And Their Correlations To Genetics Biology Essay

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'Disease does not occur unexpectedly, it is the result of constant violation of Nature's laws. Spreading and accumulation of such violations transpire suddenly in the form of a disease - but it only seems sudden'

Hippocrates

Diabetes mellitus is a metabolic disease, Pocock et al (2006) describe, resulting from a lack of or reduced effectiveness of endogenous insulin. Diabetes can cause serious microvascular (nephropathy, retinopathy and neuropathy) and macrovascular (renal-vascular disease, stroke, limb ischemia and heart disease) complications.

There are many theories surrounding diabetes one of which is the thrifty gene hypothesis (Wikipedia, Date Unknown), which stipulates that we have a gene that historically enabled us to store food in times of plenty so we could survive in famine. As famine is no longer part of our western lifestyle, and it could be argued our western lifestyle violates Natures laws, this thrifty gene serves only to make us obese - a key factor in Type 2 diabetes. Whilst it is a precursor for Type 2 diabetes, its only role in microvascular disease is as a precursor for Type 2 diabetes development.

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Diabetes can be split into two irreversible types - 1 and 2. Type 1 is usually juvenile onset which is caused by an insulin deficiency caused by Beta pancreatic islets autoimmune destruction (Cobbold 2011). Type 2 is caused by reduced insulin secretion and increased insulin resistance, and is heavily correlated with obesity, alcohol excess, but also has and 75%-85% concordance in identical twins, in comparison to 25%-35% concordance in Type 1 (Pocock et al, 2006). This is suggestive of a stronger genetic correlation in Type 2 diabetes than Type 1.

There is also gestational diabetes, a normally reversible form of diabetes experienced in pregnant women, which can cause low birth weight of the child among other symptoms (Cobbold 2011).

Pre diabetic states also exist (Cobbold (2011), Wikipedia (Date unknown) and Pocock et al(2006))- impaired glucose tolerance which is classified as a fasting glucose of between 7.8mmol and 11 mmol and impaired fasting glucose which is classified as a fasting glucose between 6 mmol and 7 mmol.

Type 2 diabetes , genetics and macrovascular/ microvascular complications do have somewhat of a 'chicken or egg' element to them. This is because many genes associated with Type 2 diabetes are also interlinked with the vasculature. For example Pocock et al (2006) help us understand that stress in the Beta islets can be the result of vascular events endogenous to the pancreas and possibly be a cause for Type 2 diabetes. The genetic element of Type 2 diabetes cannot be disputed. However do genetics also predispose to certain microvascular manifestations of Type 2 diabetes?

Diabetic neuropathy is a common condition arising from diabetes occurring in 1 in 3 Type 2 diabetics (Wikipedia (Date unknown). It is associated with a loss of sensation and absence of ankle jerks. Amputations of the feet are relatively common Boulton et al (1998) explain, with this particular diabetic manifestation.

Normal vascular function and a reasonable blood flow are essential for normal nerve function (Wikipedia (Date unknown) and Pocock (2006)). Diabetic neuropathy starts with vasoconstriction and as it progresses this vasoconstriction leads to reduced nerve function. This in turn leads to endothelial and epithelial abnormalities such as hyperplasia which can induce hypoxia. This hypoxia progresses to cause peripheral ischemia which is the cause of the characteristic diabetic foot (Wikipedia, Date unknown).

Much research has been carried out to determine if a link between genetics and neuropathy exists - and it has been determined this is unlikely. Boulton et al (1984) actually found in there control-criterion study that in contrast to genetics being a cause for diabetic neuropathy, it is hyperglycaemia and elevated serum glucose that appears to be the primary precursor for diabetic neuropathy.

Diabetic retinopathy results from microvascular retinal changes Ulhmann et al (2006) discuss. Fundamentally there are changes in the retinal - blood barrier that increase retinal vasculature permeability and change the barriers morphology.

Retinal vessels are susceptible to accumulations of fructose and glucose, and these accumulations damage the vessels of the eye. Diabetic retinopathy starts as micro aneurysms in the capillaries and can develop to macular oedema where the damaged vessels leak fluid onto the macula and blur the patient's vision. With respect to the genetics of diabetic retinopathy Uhlmann et al (2006) explains how because of racial and ethnic correlates, it can be assumed there is a link between genetics and diabetic retinopathy development. Uhlmann et al (2006) highlight several key genes that may should be studied further namely they state, 'advanced glycation end products receptor, vascular endothelial growth factor, intercellular adhesion molecule 1, beta3-adrenergic receptor gene, hemochromatosis, and alpha2beta1 integrin'.

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Diabetic nephropathy starts with microalbuniuria when there is an excess of serum albumin in the urine (Pocock et all (2006) and Wikipedia (Date unknown) . It's characterized by glomerular hypertension and a continually reducing glomerular filtration rate. With progression there is glomerular destruction, with increasing amounts of albumin in the urine. Diabetic nephropathy is one of the leading causes of end stage renal disease Parving et al (1996) explain.

Diabetic nephropathy susceptibility is multifactorial, Parving et al (1996) continue to explain, and low stature and birth weight have a part to play. This is suggestive that genetics do have a role to play in the development, further more highlighted by the differing susceptibility between ethnic groups.

To conclude, genetics are known to play a part in Type 2 diabetes -'the disease'. However there is still much to know regarding the genetics of diabetes microvascular manifestations. Both diabetic nephropathy and retinopathy would appear to have some genetic correlation regarding their occurrence, which has become apparent through twin studies, family studies and adoption studies. Conversely there does not appear to be such a link between genetics and diabetic neuropathy. This can be comprehended as the damaging factor in retinopathy and nephropathy is broadly and simplistically caused by the physical presence of sugar glucose accumulations in the retinal- blood barrier and glucose damage to the glomerulus. In comparison neuropathy is broadly and simplistically caused by the physiological factors of having hyperglycaemia, and hyperglycaemias effect on the body.