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However, some common factors that we know to be involved are: 1. Diabetes : High blood sugar levels over time can damage the vagus nerve and 'pacemaker' cells in the stomach muscles.
Type 1 diabetes risk factors aren’t as clear as those for other types of diabetes. But there are some factors we know are associated with a higher risk for this type of diabetes: Genetics.
In the early days of insulin treatment for type 1 diabetes there was much debate as to whether strict control of hyperglycaemia would delay or prevent the long-term complications of diabetes. The work of Pirart [ 50 ] suggested that microvascular complications of diabetes were less likely to occur in individuals with better glycaemic control.
In fact, diabetes mellitus has been named as the most common known cause of gastroparesis, as high levels of blood glucose may effect chemical changes in the nerves. [24] The vagus nerve becomes damaged by years of high blood glucose or insufficient transport of glucose into cells resulting in gastroparesis. [ 2 ]
Obesity has been found to contribute to approximately 55% of cases of type 2 diabetes; [10] chronic obesity leads to increased insulin resistance that can develop into type 2 diabetes, [11] most likely because adipose tissue (especially that in the abdomen around internal organs) is a source of several chemical signals, hormones and cytokines, to other tissues.
A new study published in 'Nutrition & Diabetes' suggests that eating large meals after 5 p.m. could raise your risk for type 2 diabetes. Here's what to know.
Risk factors for insulin resistance include obesity, sedentary lifestyle, family history of diabetes, various health conditions, and certain medications. Insulin resistance is considered a component of the metabolic syndrome. There are multiple ways to measure insulin resistance such as fasting insulin levels or glucose tolerance tests, but ...
Shortage of insulin [3] Risk factors: Usually type 1 diabetes, less often other types [1] Diagnostic method: High blood sugar, low blood pH, high ketoacid levels [1] Differential diagnosis: Hyperosmolar nonketotic state, alcoholic ketoacidosis, uremia, salicylate toxicity [4] Treatment: Intravenous fluids, insulin, potassium [1] Frequency
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