An insulin pump is a small machine that gives you small, steady doses of insulin throughout the day. You wear one type of pump outside your body on a belt or in a pocket or pouch. The insulin pump connects to a small plastic tube and a very small needle. You insert the needle under your skin and it stays in place for several days. Insulin then pumps from the machine through the tube into your body 24 hours a day. You also can give yourself doses of insulin through the pump at mealtimes. Another type of pump has no tubes and attaches directly to your skin, such as a self-adhesive pod.

Thank you for explaining just how things work. I have just (2months ago)gone off Diabetes Type 2 medication. BGLs around 7-10 now. It looks like I replace the rolled oats for cauliflower for breakfast and the three slices of wholegrain sourdough bread for veggies. Those two items were the continued delaying function. I’ll be on my way to decreasing the BGLs to normal, now. I have lots of fat from cold pressed virgin olive oil in my home-made hummus and over the veggies. I can look forward to the soya coffee with no guilt.
Chronic exposure of β-cells to triacylglycerol or fatty acids either in vitro or in vivo decreases β-cell capacity to respond to an acute increase in glucose levels (57,58). This concept is far from new (59,60), but the observations of what happens during reversal of diabetes provide a new perspective. β-Cells avidly import fatty acids through the CD36 transporter (24,61) and respond to increased fatty acid supply by storing the excess as triacylglycerol (62). The cellular process of insulin secretion in response to an increase in glucose supply depends on ATP generation by glucose oxidation. However, in the context of an oversupply of fatty acids, such chronic nutrient surfeit prevents further increases in ATP production. Increased fatty acid availability inhibits both pyruvate cycling, which is normally increased during an acute increase in glucose availability, and pyruvate dehydrogenase activity, the major rate-limiting enzyme of glucose oxidation (63). Fatty acids have been shown to inhibit β-cell proliferation in vitro by induction of the cell cycle inhibitors p16 and p18, and this effect is magnified by increased glucose concentration (64). This antiproliferative effect is specifically prevented by small interfering RNA knockdown of the inhibitors. In the Zucker diabetic fatty rat, a genetic model of spontaneous type 2 diabetes, the onset of hyperglycemia is preceded by a rapid increase in pancreatic fat (58). It is particularly noteworthy that the onset of diabetes in this genetic model is completely preventable by restriction of food intake (65), illustrating the interaction between genetic susceptibility and environmental factors.
Note that these medications used to treat type 2 diabetes are typically not used in pregnant or breastfeeding women. At present the only recommended way of controlling diabetes in women who are pregnant or breastfeeding is by diet, exercise, and insulin therapy. You should speak with your health-care professional if you are taking these medications, are considering becoming pregnant, or if you have become pregnant while taking these medications.
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