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Production Assistant, Diabetes In Control

International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #150: Glucose Toxicity Part 6

Clinical significance of glucose toxicity: After diagnosis of type 1 diabetes, initiation of insulin therapy induces partial clinical remission in ∼30% of the patients during the first year. This honeymoon period is characterized by normoglycemia, recovery of endogenous insulin secretion, and by improved insulin sensitivity. Although correction of several alterations secondary to insulin deficiency, such as increased counterregulatory hormone secretion, hyperosmolarity, acidosis, electrolyte changes and high free fatty acids could contribute to normalization of insulin secretion and sensitivity, reversal of glucose toxicity may also be of importance for the occurrence of remission.

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SGLT-2 Concerns

What is your top concern when prescribing SGLT-2 inhibitors to patients with diabetes?

- Amputation risk
- Infection risk
- Kidney risk
- Price

Follow the link and see how you compare to your colleagues.

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Avoiding Hypoglycemia with MDI

Which of the following is an important consideration when giving a post-meal insulin bolus with the aid of CGM-based trend arrows dosing in order to avoid hypoglycemia in persons using multiple daily insulin therapy?

A. Always consider using the full dose suggested by calculations based on the correction factor and target glucose.
B. Give ~50% of the calculated insulin dose (using the correction factor and target glucose) to adjust for active insulin (insulin on board).
C. Use ~25% of the calculated insulin dose (using the correction factor and target glucose) to adjust for active insulin (insulin on board).
D. Use 75% of the calculated insulin dose (using the correction factor and target glucose) to adjust for active insulin (insulin on board).
E. Another insulin dose should never be given after eating.

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International Textbook of Diabetes Mellitus, 4th Ed., Excerpt #149: Glucose Toxicity Part 5

The effects are consistent with a role for O-GlcNAc in damping acute hormone- and phosphorylation-mediated signals in situations of chronic nutrient excess. Although discovered in the context of diabetes, the aforementioned changes mediated by the HBP can also be viewed as adaptive responses to excess nutrient flux: muscle cells protect themselves from excess glucose fluxes and the excess nutrients are eventually stored as fat. Indeed, if insulin signaling were not dampened and glycogen synthesis were effectively engaged even with overeating, a pound of ingested carbohydrate would result in approximately four pounds of hydrated glycogen in muscle, and it is easy to visualize diets rich in sodas and donuts resulting in the development of glycogen storage diseases.

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