Type 2 Diabetes Melitus

  Diabetes have been reported to affects about 422 million adults people globally since disclosure, and consistently every day someone new is diagnosed. This is anticipated to be 366 million people by 2030, with a projection of 7,020,000 to 18,234,000 in Africa. Diabetes has been categorised majorly into two; Type 1 diabetes mellitus known as insulin-dependent diabetes, and Type 2 diabetes mellitus. Other categories include gestational diabetes which is common to pregnant women, and diabetes secondary to other causes.

  Type 2 diabetes, also know as noninsulin-dependent diabetes or adult-onset diabetes, is the most predominant class (about 90-95%) of chronic heterogeneous group of metabolic disorders characterized by hyperglycemia which compensate impaired insulin action and/or inadequate compensatory secretion response. Its chronic complications include retinopathy, nephropathy, neuropathy, foot amputations, and macrovascular complications. Unlike Type 1, Type 2 diabetes is not caused by autoimmune destruction of the pancreatic β cells, but appears to be caused by a number of different defects in both insulin action and insulin secretion. T2D usually develops after the age of 40. Hence, it is also known as “adult diabetes mellitus”.

Pathophysiology in T2DM diagram providedby ResearchGate
Pathophysiology in T2DM (diagram provided by ResearchGate)
Complications of Type 2 diabetes


  • Sudden weight loss
  • Blurry vision
  • Frequent thirsty and urination
  • Delayed wounds healing
  • Tingling hands/feet
  • Sexual problems
  • Vaginal infections


   Type 2 diabetes is a multifactorial disorder with a burden of life threatening complications. For simplicity, the harmful impacts of hyperglycemia are classified into macrovascular, and microvascular complications.

1. Microvascular complications of T2D: Hyperglycemia cause visual impairment,
kidney failure, and other serious problems, such as nerve damage that can demand amputations of the limbs. These complications are categorized as the microvascular complications of diabetes. This include:

  • Diabetes nephropathy which is an interminable diabetes complication that specifically affect the kidney. It result from damage to the convoluted capillaries in the nephron of a kidney which function to remove certain substances from the blood before it flows into the convoluted tubule. This complication is the leading cause of renal failure in the United State. It is described by nephrotic syndrome and diffuse scarring of the glomeruli, and defined by proteinuria (> 500 mg of protein in the urine produced by diabetic in 24 hours) followed by reduction in the concentration of proteinuria, or “microalbuminuria.” (30–299 mg of albumin in urine produced by diabetes patient in 24 hours). High blood pressure, High levels of blood urea nitrogen (BUN) and serum creatinine, morning sickness, nausea, vomiting, ankle and leg swelling, and leg cramps have been reported in diabetes-related nephropathy. The mechanism through which diabetes caused nephropathy is well established. Elevated blood glucose level caused an increased in the filtration, and intensified the pressure on the filters. This later expand the diameter of the glomeruli sive, thus resulting in leakage of substances, mainly protein, into the urine. It is critical to note that conditions such as urinary tract infections, exercise, and hematuria may cause a falseful increased in the level of protein in the urine.
  • Neuropathy, which is the term used to portray a problem associated
    with the peripheral nerves. Neuropathy caused by hyperglycemia is termed Diabetic neuropathy. Symptoms seen in diabetic with neuropathy incorporate pain, tingling and numbness while no symptom is reported in others. Sensory, autonomic and motor neuropathies make up the family of nerve disorders caused by diabetes. The precise framework of how hyperglycemia caused peripheral nerves injury is not well established but rather accepted to be closely related to mechanisms such as polyol accumulation (e.g., hydrogenated starch hydrolysates, erythritol, isomalt, lactitol, etc.), injury from advanced glycation end products (AGEs), and oxidative stress. The small blood vessels supply the
    nutritional demand of the nerve cells. Elevated blood glucose level damaged the nerve fibres and eventually damaged the pathway for the generation of electrochemical nerve impulses. This consequently brings about weak sensation, development, organ or organ work, or different parts of
    wellbeing, contingent upon the type of nerve damaged; sensory, autonomic or motor. Treatment of autonomic neuropathy is focused towards the affected organ framework, and additionally incorporates advancement of glycemic control.
  • Retinopathy, a prominent microvascular complication of diabetes. About 10,000 visual impairment is annually reported in the United State. Advancement of diabetic retinopathy in type 2 diabetics was observed to be related to both severe hyperglycemia and the occurrence of hypertension. There are several proposed pathological mechanisms by which diabetes may lead to development of retinopathy. Sugar alcohol accumulation has been linked to microaneurysm formation, thickening of basement membranes, and loss of pericytes. Growth factors, including vascular endothelial growth factor
    (VEGF), growth hormone, and transforming growth factor β, have likewise been hypothesized to assume vital roles in the development of diabetic retinopathy. Damage by glycoproteins, and oxidative stress may likewise play an essential role in cellular injury from high blood sugar.

2 Macrovascular complications of T2D: Macrovascular diseases mainly affect the large blood vessels. Macrovascular complexities, generally particular to diabetes, incorporate coronary heart disease (CAD), cerebrovascular disease (CBVD) and peripheral vascular disease or polyvascular disease (PVD). However, not all macrovascular complications are subsequent of diabetes. Diabetes exasperate the risk of developing macrovascular complications by 2–4 times. Macrovascular diseases in type 2 diabetes mellitus are frequently viewed in cluster, without separation into the components that make up MVD. This is due to the fact that one component precede the other, and furthermore the interrelationship between the fractions of macrovascular diseases (Giuseppe et al., 2013). PVD, CAD and CBVD are comparable and typical risk factors for atherosclerosis. The narrowing (reduced in the diameter) of the arterial blood vessels, a characteristic of atherosclerosis, is the focal obsessive component in macrovasular diseases. This might be as a result of chronic inflammation and injury to the arterial wall of the blood vessel in the peripheral or coronary vascular framework. in response, oxidized lipids from LDL particles accumulate in the endothelial wall of arteries. Angiotensin II advances the oxidation of such particles. Monocytes then invade the arterial wall and differentiate into macrophages, which aggregate oxidized lipids to form froth cells. macrophage proliferation is then stimulated and attract T- lymphocytes. consequently, smooth muscle proliferation, collagen formation, and accumulation are induced. thus, a fibrous, atherosclerotic injury is formed. An intense vascular localized necrosis comes about because of the ruption of this sores. In addition to the increased in the degeneration of the walls of the arteries caused by accumulated fatty deposits and scar tissue, vascular impediment and cardiovascular occasions comes about because of the blend of expanded coagulability and impaired fibrinolysis. These may be as an aftereffects of weakened nitric oxide generation, increased free radical formation in platelets, and an altered calcium control reported to increase the concentration of plasminogen activator inhibitor. Although the precise regular course of procedure through which diabetes escalate atherosclerotic plaque formation are yet to be completely uncovered. Evidence has shown that diabetes increase the likelihood of developing cardiovascular disease (CVD). Other contributing factors that can likewise act to advance CVD includes hyperlipidemia, abdominal obesity, increased coagulability, and hypertension. CVD is the main driving force behind death in both type 1 or type 2 diabetics, and accounts for the larger component of medical care expenditures in individuals with diabetes. People with type 2 diabetes have a much higher risk (about 150-400%) of developing stroke. The likelihood of intermittent dementia, and in addition mortality, is hoisted in patients with diabetes. Thus, type 2 diabetes is a solid autonomous indicator of the likelihood of cerebrovascular disease and stroke, as in coronary artery disease.


   Presently, scientists are still strungling to provide cure for the two major categories of diabete mellitus. The life-threatening co-morbidities of diabetes which includes obesity, cataract, micro- and macro- vascular complications made it an outstanding societal problem, and about 5–10% of the annual medical care budget in many countries is disbursed on its management. However, no medication has been designed to cure T2D.

    Thiazolidinediones (TZDs) reported to address the core problem (cell insensitivity) in T2D do so by activating PPARγ which regulate the transcription of genes (adipocyte fatty acid-binding protein, lipoprotein lipase, and phosphoenolpyruvate carboxy kinase in adipose tissue), and the up-regulation of acyl-Co synthetase, fatty acid transporters, and uncoupling protein-2, involved in metabolism and proliferation of adipocytes, but unfortunately, abandoned in some countries due to their associated life-threatening side effects, which in some cases more fatal than the complications of diabetes itself. The huge worldwide health burden of T2D and the failure of many therapeutic agents in its treatment due to their associated side effects remained evidence for an urgent need of new puissant antidiabetic agents with zero or minimal side effects. However, diabetes can still be keep in checked.


  • Feed on low glycemic food such as egg, cherries, avocados, natural milk, nuts, berries,
  • No sedentary lifestyle. Exercise regularly!
  • No consumption of alcohol and no smoking,
  • Feed more on probiotics,
  • Feed less on refined carbohydrates and increase your intake of fibre,
  • Avoid been stressed up and get adequate sleep to manage blood sugar spikes & dips, and
  • Avoid artificial sweeteners.


To live an healthy life with no risk of diabetes, ensure you feed more on grains, get plenty of fibres, avoid fad diet, exercise regularly, and ensure you keep a good watch on your blood glucose level by going for frequent medical checkup. I wish you healthy lives!

Written and published by BLESSING AYOKUNLE