Male, 68 years of age, type 2 diabetes, Italian, on long-acting insulin and GLP-1. Basal glucose levels are within target as are most post-prandials except every night after dinner. We have talked several times about lowering carbs, which he has done during the daytime, but has difficulty cutting back on dinner meal. We had in the past discussed taking rapid-acting insulin for meals, but he refused. After two weeks, patient sent me his CGM results. Even he started getting concerned about his evening post-prandial levels. Rapid-acting insulin added before dinner and post-prandials are now in target range. He has not once complained about taking the rapid-acting insulin before dinner.

In this week's Homerun Slides, a focus on CGM outcomes.

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.

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.

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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In this week's Homerun Slides, we begin a new series showing the value of continuous glucose monitoring.

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.

Holistic approach revised, but there is still more to be done to individualize treatment.

A1c management over longer periods shown to decrease likelihood of diagnosis.

New SGLT1/SGLT2 inhibitor lowers HbA1c and has less hypoglycemia episodes among people who have type 1 diabetes.