Peer Responses:

    Length: A minimum of 150 words per post, not including references
    Citations: At least one high-level scholarly reference in APA per post from within the last 5 years
    Citations need to be within 5 (Five)  years
    Context: Nursing in the USA
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            Type II Diabetes Mellitus is a non-insulin dependent type of diabetes. This type of diabetes can occur at any age, however its risk of development increases with age, usually affecting those 40 years of age and older, the obese, and may involve some racial and genetic predispositions (Dlugasch & Story, 2021). In this condition there is insulin resistance related to insulins inability to act on target insulin-sensitive tissues like fat, muscle and the liver, causing a lack of glucose cellular use (Dlugasch & Story, 2021). In response, the liver produces more glucose, a process called gluconeogenesis, further adding to the hyperglycemia (Dlugasch & Story, 2021). This hyperglycemia then triggers more insulin production, a compensatory hyperinsulinemia response, for which pancreatic beta cells struggle to maintain; eventually leading to beta cell failure and a decline in insulin secretion (Dlugasch & Story, 2021). Fortunately, through lifestyle modifications, diet and exercise, insulin responsiveness can be improved, leading to a better control of blood glucose and diabetes.
            Additionally, other cellular level changes thought to play a role in diabetes have been observed. It is well known that obesity is highly related to the development of type II diabetes, and its effects on the body, explained below, might explain obesitys influence in the development of diabetes. In obesity, free fatty acids are extremely high, and this impairs glucose cellular uptake and decreases insulin secretion (Dlugasch & Story, 2021). Fat cells or adipocytes, plentiful in obesity, also release adipokines like leptin, which is increased in diabetes and may cause overeating, and the release of other systemic inflammatory chemicals, which can cause further damage to pancreatic islet cells, complicating ones diabetes (Dlugasch & Story, 2021). Additionally, the hormone amylin is also co-secreted with insulin by the beta cells, which can leave amyloid deposits outside beta cells, also further contributing to islet cell destruction (Dlugasch & Story, 2021). Lastly, as hyperglycemic control progresses and worsens, and when a diabetic experiences extreme hyperglycemia, further pathophysiologic changes occur, which could be potentially life-threatening.
            Reference
Dlugasch, L., & Story, L. (2021). Applied pathophysiology for the advanced practice nurse. Burlington, MA: Jones & Bartlett Learning.