Harmonizing to the World Health Organisation diabetes mellitus is a province of chronic hyperglycemia due to familial and environmental factors. In type 1 diabetes mellitus there is no production of insulin whereas In type 2 diabetes mellitus there is deficient insulin or cells do non react to insulin present in the organic structure ( insulin opposition ) ( 1 ) . The most frequent signifier is type 2 diabetes that accounts for more than 85 % of instances, with type 1 diabetes accounting for 10 % of instances, specific and gestational diabetes with 5 % of instances ( 2 ) .
WHO besides estimates that more than 180 million people worldwide have diabetes mellitus and this figure will most probably more than double by 2030 without pressing action. In 2005 an estimated 1.1 million people died from diabetes and 80 % of these deceases occurred in low and in-between income states such as Zimbabwe, half of these people being under the age of 70 and 55 % being adult females ( 2 ) .
Before the 1990s, diabetes was considered a rare medical status in Africa. Epidemiologic surveies carried out in that decennary, nevertheless, provided grounds of a tendency toward increased incidence and prevalence of type 2 diabetes in African populations ( 3 ) . Indeed, Africa is sing the most rapid demographic and epidemiological passage in universe history. It is characterized by a enormous rise in the load of noncontagious diseases ( NCDs ) , underlined by the increasing life anticipation and lifestyle alterations ensuing from the decrease in infective diseases and increased birthrate, every bit good as Westernization ( 4 ) .
About all the studies published between 1959 and 1985 showed a prevalence of diabetes below 1.4 per centum, except those from South Africa, where higher prevalence was reported.
The prevalence of diabetes in Africa was about 3 million in 1994 ; but the part is due to see a two-to treble addition by the twelvemonth 2010 ( 5 ) . The highest prevalence is found in populations of Indian beginning, followed by black populations and Caucasians. Among the population of Indian beginning in South Africa and Tanzania, the prevalence is between 12 and 13 per centum ( 6 ) . The prevalence in inkinesss follows a Westernization gradient, with that of rural Africa by and large below 1 per centum but that of urban Africa between 1 and 6 per centum. In general the prevalence of type 2 diabetes is low in both rural and urban communities of West Africa except in urban Ghana, where a high rate of 6.3 per centum was late reported ( 7 ) . Moderate rates have been reported from South Africa: 4.8 per centum in a semi-urban community in the Orange Free State, 6.0 per centum in an urban community of the Orange Free State, 5.5 per centum in Durban ( largely occupied by the Zulu folk ) , and 8 per centum in Cape Town ( largely occupied by the Xhosa tribe. )
INSULIN AND ITS FUNCTION IN GLUCOSE METABOLISM
The major map of insulin is to keep low blood glucose degrees and counter the conjunct action of a figure of hyperglycemia-generating endocrines. Untreated upsets associated with insulin by and large lead to severe hyperglycaemia and shortened life span as in diabetes mellitus ( 1 ) . Insulin is synthesized as a preprohormone in the ?-cells of the islets of Langerhans. Its signal peptide is removed in the cisternae of the endoplasmic Reticulum and it is packaged into secretory cysts in the Golgi, folded to its native construction, and locked in this conformation by the formation of 2 disulfide bonds ( 1,8 ) . Specific peptidase activity cleaves the halfway tierce of the molecule, which dissociates as C peptide, go forthing the amino terminus B peptide disulfide bonded to the carboxy terminus A peptide. Insulin secernment from ?-cells is chiefly regulated by plasma glucose degrees ( 8 ) . Increased consumption of glucose by pancreatic ?-cells leads to a attendant addition in metamorphosis. The addition in metamorphosis leads to an lift in the ATP/ADP ratio. This in bend leads to the suppression of an ATP-sensitive K channel ( KATP channel ) . The net consequence is a depolarisation of the cell taking to Ca2+ inflow and insulin secernment ( 8 ) .
( 1,3 ) pecial transporter proteins found in cell membranes allow glucose that is in the blood to come in into a cell. These transporters are controlled indirectly by blood insulin in certain organic structure cell types like musculus cells. Low degrees of go arounding insulin, or its complete absence, will forestall glucose from come ining those cells as in typical type 1 diabetes. More normally, nevertheless, there is a lessening in the sensitiveness of cells to insulin for case the decreased insulin sensitiveness feature of type 2 diabetes, ensuing in decreased glucose soaking up. In either instance, there is cell famishment and weight loss that is sometimes utmost. In a few instances, there is a defect in the release of insulin from the pancreas. Either manner the consequence is the same and that is elevated blood glucose degrees ( 1,8 ) .
Insulin receptor activation consequences in internal cellular mechanisms that straight affect glucose consumption by modulating the figure and operation of protein molecules in the cell membrane that are responsible for transporting glucose into the cell.Muscle cells ( myocytes ) and fat cells ( adipocytes ) are the two types of tissues that are most strongly influenced by insulin, every bit far as the stimulation of glucose consumption is concerned.Myocytes are of import because of their cardinal function in motion, external respiration and circulation and adipocytes are of import because they accumulate extra nutrient energy against future demands. Together they account for about two-thirds of all cells in a typical homo organic structure ( 1,8 ) .
Insulin binds to the extracellular part of the alpha fractional monetary units of the insulin receptor. This causes a conformational alteration in the insulin receptor and there is activativation of the kinase sphere situated on the intracellular part of the beta fractional monetary units. This activated kinase sphere autophosphorylates tyrosine residues on the C-terminus of the receptor every bit good as tyrosine residues in the IRS-1 protein. Consequently the undermentioned stairss occur:
1. Phosphorylated IRS-1, in bend, binds to and activates phosphoinositol 3 kinase ( PI3K ) .
2. PI3K catalyzes the reaction PIP2 + ATP > PIP3 + ADP.
3. PIP3 activates protein kinase B ( PKB ) .
4. PKB phosphorylates glycogen synthase kinase ( GSK ) and thereby inactivates GSK.
5. GSK can no longer phosphorylate animal starch synthase ( GS ) .
6. Unphosphorylated GS makes more animal starch.
PKB besides facilitates cyst merger, ensuing in an addition in GLUT4 transporters in the plasma membrane.After the signal has been produced, expiration of signaling is needed and this can be by debasement and endocytosis of the receptor edge to insulin. In add-on, signaling can be terminated by dephosphorylation of the tyrosine residues by tyrosine phosphatases. Serine/Threonine kinases are besides known to cut down the activity of insulin. Finally, with insulin action being associated with the figure of receptors on the plasma membrane, a lessening in the sum of receptors besides leads to expiration of insulin signaling ( 1,8,9 ) .
In add-on to its function in modulating glucose metamorphosis, insulin stimulates lipogenesis, diminishes lipolysis, and increases amino acerb conveyance into cells. Insulin besides modulates written text, changing the cell content of legion messenger RNA. It stimulates growing, DNA synthesis, and cell reproduction, effects that it holds in common with the insulin-like growing factors ( IGFs ) and relaxin. ( 1,9 ) .
DIAGNOSIS AND MONITORING OF DIABETES MELLITUS
Different trials can be used to name and supervise blood glucose degrees in diabetes mellitus patients and these include random and fasting blood glucose, unwritten glucose tolerance trial, blood carbamide, blood H, urinary protein, blood insulin, blood fructosamine and glycosylated hemoglobin ( HbA1c ) ( 1 ) .
For diagnosing the OGTT, fasting and random blood glucose trials are ideal and harmonizing to the WHO guidelines, if the plasma glucose is & A ; lt ; 5.5 mmol/L so diabetes is improbable. A fasting plasma glucose of 7.0 mmol/L or more, or a random glucose of 11.1 mmol/L or more makes diabetes likely and the diagnosing is confirmed by a repetition unnatural trial. If the plasma glucose is between 5.5 and 6.9 mmol/L fasting, or between 5.5 and 11.0 mmol/L non-fasting, an OGTT with 75 g anhydrous glucose is recommended. ( 1 )
Blood H, blood carbamide and urinary protein, can besides be used in diagnosing of diabetes but merely as non specific confirmatory trials for fasting, random blood glucose and OGTT.Blood Insulin is seldom measured in diagnosing of diabetes mellitus ( 1,8 ) .
In the direction and control of diabetes, blood glucose determined at the clip of the clinic attending can merely give limited information and may non stand for the overall intimacy of control at other times therefore it has restrictions in supervising glucose control. The HbA1c trial provides a better index of diabetic control than plasma glucose since it is non greatly affected by short-run fluctuations in plasma glucose ( 8 ) .
GLYCOSYLATED HAEMOGLOBIN AND ITS IMPORTANCE
HbA1c is a signifier of hemoglobin used chiefly to place the mean plasma glucose concentration over drawn-out periods of clip ( three to four months ) . In the normal 120 twenty-four hours lifetime of the ruddy blood cell glucose molecules fall in to haemoglobin in a non enzymatic reaction organizing HbA1c.In persons with ill controlled diabetes, additions in the measures of the glycosylated hemoglobin have been noted ( 10,11 ) . Once a hemoglobin molecule is glycosylated, it remains that manner. A build up of HbA1c within the ruddy blood cell reflects the mean degree of glucose to which the cell has been exposed during its life rhythm ( 1,8 ) .
Measuring HbA1c assesses the effectivity of therapy by supervising long term plasma glucose ordinance. Monitoring of glycogenic position is considered a basis of diabetes attention and affects how doctors and patients adjust medical therapy every bit good as behavioral therapy ( diet and exercising ) ( 11,12 ) . It has been shown in a randomized survey that when wellness attention suppliers and patients are informed about the HbA1c consequences blood glucose control is improved. Simply cognizing the consequences improves glycemic control, either through improved attempts by the patient or by the supplier ( 10 ) .
GLUCOSE CONTROL IN DIABETICS
In a diet control survey done among diabetics with HbA1c consequences available in the United States it was shown that, 39 % had good control ( HbA1c & A ; lt ; 7 % ) 36 % had suboptimal control ( HbA1c 7-9 % ) and 25 % had hapless control ( HbA1c & A ; gt ; 9 % ) ( 13 ) .
Public wellness research labs in Zimbabwe do non offer the HbA1c check for diabetic patients. Many patients are from hapless socio-economic background and rely entirely on public wellness installations as they can non afford private health care installations. Therefore, most Zimbabwean diabetics do non hold any signifier of long term monitoring of their blood glucose degrees and are at a hazard of holding high degrees of HbA1c degrees without them or their wellness attention suppliers cognizing it.
INCREASED HbA1c AND COMPLICATIONS OF DIABETES MELLITUS
A certain survey showed that an mean HbA1c degree of 7.2 % resulted in a 76 % decrease in retinopathy, a 60 % decrease in neuropathy, a 50 % decrease in kidney disease and a 35 % decrease in cardiovascular disease. ( 9,14 ) . Another survey in America demonstrated unambiguously that keeping near normal blood glucose degrees significantly lowers a individual ‘s hazard of developing complications related to diabetes ( 9 ) .
In a survey done to find the relationship of HbA1c degrees to hospital admittance of patients, it was found that the likeliness of admittance increased with higher HbA1c degrees. The figure of admittances of diabetic patients with HbA1c degrees in the scope ( 10.8 % – 18.4 % ) was higher with 5 481 admittances in a 3 twelvemonth period compared with 2 566 admittances of patients with HbA1c degrees in the mention part of 7.7 % – 8.1 % ( 11 ) .