They Won't Teach You This in School: Education in Type 2 Diabetes Mellitus, a Social Media Campaign

Etiology And Risk Factors

As a multifactorial disease, the causes of DM2 involve genetic, metabolic, and environmental factors:

• ●

  The genetic factor can be seen in people with first-degree relatives with DM2, they have a 5-10 times higher risk of developing the disease. There are at least 100 genes associated with a low or moderate risk of developing DM2 and some interfere with insulin secretion (McCulloch, 2019).

• ●

  Metabolic and environmental factors sometimes are related. A sedentary lifestyle and visceral obesity lead to a higher risk of having this disease since more than 80% of the cases of DM2 are associated with obesity. Weight loss along with diet changes have been shown to reduce insulin resistance and improve glucose tolerance. (Abbas, 2015).

• ●

  A BMI of ≥25 Kg/m2, classified as overweight, and the lack of physical inactivity can be considered as decisive factors. Other determinants: ethnicity, a previously identified IFG (impaired fasting glucose) or A1c (glycated hemoglobin) of 5.7 to 6.4%, history of gestational DM or giving birth to a child with a birth weight >4kg, hypertension (≥140/90 mmHg), HDL cholesterol concentration <35 mg/100 mL (0.90 mmol/L), triglyceride concentration >250 mg/100 mL (2.82 mmol / L) or both, medical history of polycystic ovary syndrome or acanthosis nigricans, as well as cardiovascular disease background (Jameson, 2018).

Pathophysiology

In most cases, multiple genes responsible for pancreatic development and insulin synthesis, secretion, or activity are involved while monogenic DM2 rarely occurs. Some of which are frequently associated with the development of the disease are listed below:

• ●

  SLC30A8 (Solute Carrier Family 30 Member 8), HHEX/IDE (Homeobox, hematopoietically expressed; Insulin-degrading enzyme), and KCNJ11 (Potassium Inwardly rectifying channel subfamily J member 11), involved in the development of β cells (McCulloch, 2019).

• ●

  Polymorphisms in the TCF7L2 gene (transcription factor 7-like 2) have been associated with an increased risk of DM2.

• ●

  Mutations in MODY 2 and MODY 4 (Maturity Onset Juvenile Diabetes), although they rarely occur, have an autosomal dominant inheritance pattern and are associated with insulin resistance and its altered secretion, mainly in people inside the normal weight range and under 25 years of age (Chatterjee, 2017).

Metabolic defects are associated with insulin resistance, due to an altered response of peripheral tissues to insulin, especially skeletal muscle, adipose, and liver tissue. This results in the inability to inhibit gluconeogenesis in the liver, causing high fasting blood glucose levels. Additionally, smooth muscle glucose uptake and glycogen synthesis after a meal are impaired, leading to postprandial glycemia. The inhibition of lipase protein activity in adipose tissue is also affected, which causes an accumulation of free fatty acids and in turn amplifies the state of insulin resistance. Finally, there is a reduction in the expression of GLUT4 transporter on the surface of skeletal muscle cells. It is known that one of the mechanisms by which physical activity improves glucose sensitivity is by increasing GLUT4 (Gaster, 2001).

In the early stages of the disease, β cell function increases to counteract insulin resistance and maintain euglycemia. However, as the disease progresses, β cells’ ability to adapt to the disease’s long-term demands is depleted, inducing a transition to a state of relative insulin deficiency (Gaster, 2001).