Real-World Evidence of Automated Insulin Delivery System Use.

Objective: Pivotal trials of automated insulin delivery (AID) closed-loop systems have demonstrated a consistent picture of glycemic benefit, supporting approval of multiple systems by the Food and Drug Administration or Conformité Européenne mark receipt. To assess how pivotal trial findings translate to commercial AID use, a systematic review of retrospective real-world studies was conducted. Methods: PubMed and EMBASE were searched for articles published after 2018 with more than five nonpregnant individuals with type 1 diabetes (T1D). Data were screened/extracted in duplicate for sample size, AID system, glycemic outcomes, and time in automation. Results: Of 80 studies identified, 20 met inclusion criteria representing 171,209 individuals. Time in target range 70-180 mg/dL (3.9-10.0 mmol/L) was the primary outcome in 65% of studies, with the majority of reports (71%) demonstrating a >10% change with AID use. Change in hemoglobin A1c (HbA1c) was reported in nine studies (range 0.1%-0.9%), whereas four reported changes in glucose management indicator (GMI) with a 0.1%-0.4% reduction noted. A decrease in HbA1c or GMI of >0.2% was achieved in two-thirds of the studies describing change in HbA1c and 80% of articles where GMI was described. Time below range <70 mg/dL (<3.9 mmol/L) was reported in 16 studies, with all but 1 study showing stable or reduced levels. Most systems had >90% time in automation. Conclusion: With larger and more diverse populations, and follow-up periods of longer duration (∼9 months vs. 3-6 months for pivotal trials), real-world retrospective analyses confirm pivotal trial findings. Given the glycemic benefits demonstrated, AID is rapidly becoming the standard of care for all people living with T1D. Individuals should be informed of these systems and differences between them, have access to and coverage for these technologies, and receive support as they integrate this mode of insulin delivery into their lives.

Endurance Exercise Performance Is Reduced after 6-h Dives at 1.35 ATA When Breathing 100% Oxygen Compared with Air.

INTRODUCTION: Long-duration dives on consecutive days reduces muscular performance, potentially affecting military personnel. However, a paucity of data exists on how breathing gases affect endurance performance. This study examined the influence of long-duration diving with different breathing gases on aerobic endurance and handgrip performance. METHODS: Twenty-three military divers completed a single 6-h dive (single dive [SD]) and five 6-h dives over consecutive days (dive week [DW]) with 30-min cycling intervals using air (AIR, n = 13) or 100% oxygen (OXY, n = 10). Before and after SD and DW, subjects completed a maximum handgrip strength test, a handgrip endurance test at 40% maximal strength, and a time to exhaustion run. RESULTS: Handgrip endurance decreased after DW in OXY (SD, 1.9 ± 0.0 vs 1.4 ± 0.3 min) compared with AIR (1.8 ± 0.0 vs 1.8 ± 0.2 min) ( P < 0.001). Run time decreased after SD (Pre, 20.7 ± 10.4 min; Post, 16.6 ± 7.6 min; P = 0.039) and DW (Pre, 21.6 ± 9.0 min; Post, 11.2 ± 4.0 min; P < 0.001) in OXY and after overall diving in AIR (Pre, 26.5 ± 10.2 min; Post, 22.3 ± 7.5 min; P = 0.025). V̇O 2 decreased after diving only in AIR (Pre, 42.6 ± 3.4 mL·kg -1 ⋅min -1 ; Post, 40.4 ± 3.7 mL·kg -1 ⋅min -1 ; P = 0.010). There were no other significant effects. CONCLUSIONS: Breathing 100% oxygen during long-duration dives on consecutive days may exacerbate decreases in aerobic endurance and impairs handgrip endurance compared with air. Additional research is needed to elucidate mechanisms of action and possible mitigation strategies.

Loss of renal olfactory receptor 1393 leads to improved glucose homeostasis in a type 1 diabetic mouse model.

Renal olfactory receptor 1393 (Olfr1393) is an understudied sensory receptor that contributes to glucose handling in the proximal tubule. Our previous studies have indicated that this receptor may serve as a regulator of the sodium glucose co-transporters (SGLTs) and contributes to the development of glucose intolerance and hyperfiltration in the setting of diet-induced obesity. We hypothesized that Olfr1393 may have a similar function in Type 1 Diabetes. Using Olfr1393 wildtype (WT) and knockout (KO) mice along with streptozotocin (STZ) to induce pancreatic ß-cell depletion, we tracked the development and progression of diabetes over 12 weeks. Here we report that diabetic male Olfr1393 KO mice have a significant improvement in hyperglycemia and glucose tolerance, despite remaining susceptible to STZ. We also confirm that Olfr1393 localizes to the renal proximal tubule, and have uncovered additional expression within the glomerulus. Collectively, these data indicate that loss of renal Olfr1393 affords protection from STZ-induced type 1 diabetes and may be a general regulator of glucose handling in both health and disease.