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Aims/hypothesis: We assessed the impact of initiating intermittently scanned continuous glucose monitoring (isCGM) compared with capillary blood glucose monitoring (BGM) on HbA1c levels and hospitalisations for diabetes-related complications in adults with insulin-treated type 2 diabetes in Sweden. Methods: This retrospective comparative cohort study included adults with type 2 diabetes who had a National Diabetes Register initiation date for isCGM after 1 June 2017. Prescribed Drug Register records identified subgroups treated with multiple daily insulin injections (T2D-MDI) or basal insulin (T2D-B), with or without other glucose-lowering drugs. The National Patient Register provided data on hospitalisation rates. Results: We identified 2876 adults in the T2D-MDI group and 2292 in the T2D-B group with an isCGM index date after 1 June 2017, matched with 33,584 and 43,424 BGM control participants, respectively. The baseline-adjusted difference in the change in mean HbA1c for isCGM users vs BGM control participants in the T2D-MDI cohort was −3.7 mmol/mol (−0.34%) at 6 months, and this was maintained at 24 months. The baseline-adjusted difference in the change in HbA1c for isCGM users vs BGM control participants in the T2D-B cohort was −3.5 mmol/mol (−0.32%) at 6 months, and this was also maintained at 24 months. Compared with BGM control participants, isCGM users in the T2D-MDI cohort had a significantly lower RR of admission for severe hypoglycaemia (0.51; 95% CI 0.27, 0.95), stroke (0.54; 95% CI 0.39, 0.73), acute non-fatal myocardial infarction (0.75; 95% CI 0.57, 0.99) or hospitalisation for any reason (0.84; 95% CI 0.77, 0.90). isCGM users in the T2D-B cohort had a lower RR of admission for heart failure (0.63; 95% CI 0.46, 0.87) or hospitalisation for any reason (0.76; 95% CI 0.69, 0.84). Conclusions/interpretation: This study shows that Swedish adults with type 2 diabetes on insulin who are using isCGM have a significantly reduced HbA1c and fewer hospital admissions for diabetes-related complications compared with BGM control participants. [ABSTRACT FROM AUTHOR]

OBJECTIVE: We assessed the impact of intermittently scanned continuous glucose monitoring (isCGM) compared with blood glucose monitoring (BGM) on rates of hospitalization for metabolic and vascular complications of diabetes and on HbA1c levels for adults with type 1 diabetes. RESEARCH DESIGN AND METHODS: This retrospective study using data from the Swedish National Diabetes Register and the Swedish National Patient Register comprised adults with type 1 diabetes and an isCGM initiation date after 1 June 2017 and matched control individuals using BGM. Hospital admission rates were calculated per 100 person-years of follow-up. RESULTS: We identified 11,822 adults with type 1 diabetes and an isCGM index date after 1 June 2017 and HbA1c baseline values 3–8 months prior to the index date. Compared with 3,007 BGM users, isCGM users had a significantly lower relative risk of hospitalization for hypoglycemia (0.32; 95% CI 0.14, 0.74), diabetic ketoacidosis (0.55; 0.35, 0.87), stroke (0.48; 0.37, 0.64), acute myocardial infarction (0.64; 0.46, 0.91), atrial fibrillation (0.59; 0.38, 0.94), heart failure (0.25; 0.16, 0.39), peripheral vascular disease (0.21; 0.07, 0.62), kidney disease (0.48; 0.35, 0.66), or hospitalization for any reason (0.32; 0.29, 0.35). Compared with BGM users, change in mean HbA1c for isCGM users was −0.30% (−3.3 mmol/mol) at 6 months and −0.24% (−2.6 mmol/mol) at 24 months (both P < 0.001). CONCLUSIONS: This study shows that adults with type 1 diabetes in Sweden who initiate isCGM have significantly reduced hospitalization rates for acute diabetes events, kidney disease, and cardiovascular complications, along with improved glucose control, compared with BGM users. [ABSTRACT FROM AUTHOR]

Aims/hypothesis: Previous studies have shown that individuals with similar mean glucose levels (MG) or percentage of time in range (TIR) may have different HbA1c values. The aim of this study was to further elucidate how MG and TIR are associated with HbA1c. Methods: Data from the randomised clinical GOLD trial (n=144) and the follow-up SILVER trial (n=98) of adults with type 1 diabetes followed for 2.5 years were analysed. A total of 596 paired HbA1c/continuous glucose monitoring measurements were included. Linear mixed-effects models were used to account for intra-individual correlations in repeated-measures data. Results: In the GOLD trial, the mean age of the participants (± SD) was 44±13 years, 63 (44%) were female, and the mean HbA1c (± SD) was 72±9.8 mmol/mol (8.7±0.9%). When correlating MG with HbA1c, MG explained 63% of the variation in HbA1c (r=0.79, p<0.001). The variation in HbA1c explained by MG increased to 88% (r=0.94, p value for improvement of fit <0.001) when accounting for person-to-person variation in the MG–HbA1c relationship. Time below range (TBR; <3.9 mmol/l), time above range (TAR) level 2 (>13.9 mmol/l) and glycaemic variability had little or no effect on the association. For a given MG and TIR, the HbA1c of 10% of individuals deviated by >8 mmol/mol (0.8%) from their estimated HbA1c based on the overall association between MG and TIR with HbA1c. TBR and TAR level 2 significantly influenced the association between TIR and HbA1c. At a given TIR, each 1% increase in TBR was related to a 0.6 mmol/mol lower HbA1c (95% CI 0.4, 0.9; p<0.001), and each 2% increase in TAR level 2 was related to a 0.4 mmol/mol higher HbA1c (95% CI 0.1, 0.6; p=0.003). However, neither TIR, TBR nor TAR level 2 were significantly associated with HbA1c when accounting for MG. Conclusions/interpretation: Inter-individual variations exist between MG and HbA1c, as well as between TIR and HbA1c, with clinically important deviations in relatively large groups of individuals with type 1 diabetes. These results may provide important information to both healthcare providers and individuals with diabetes in terms of prognosis and when making diabetes management decisions. [ABSTRACT FROM AUTHOR]

To study the local tissue lactate production in the normal state and its possible disturbances in insulin resistance, rates of lactate release from adipose tissue (AT) and skeletal muscle (SM) were compared postabsorptively and during a hyperinsulinemic euglycemic clamp in 11 healthy nonobese and 11 insulin-resistant obese women. A combination of microdialysis, to measure interstitial lactate, and the 133Xe clearance technique, to determine local blood flow, were used. In the controls, local blood flow increased by 40% in SM (P < 0.05) and remained unchanged in AT, whereas the interstitial-plasma difference in lactate doubled in AT (P < 0.005) and was unaffected in SM during hyperinsulinemia. In the obese, blood flow and interstitial-plasma difference in lactate remained unchanged in both tissues during hyperinsulinemia. The lactate release ([micro]mol*100 [g.sup.-l]*[min.sup.-1]) was 1.17 [+ or -] 0.22 in SM and 0.43 [+ or -] 0.11 in AT among the controls (P < 0.01) and 0.86 [+ or -] 0.23 in SM and 0.83 [+ or -] 0.25 in AT among the obese women in the postabsorptive state. During insulin infusion, lactate release in the controls increased to 1.92 [+ or -] 0.26 in SM (P < 0.005) and to 1.14 [+ or -] 0.22 in AT (P < 0.005) but remained unchanged in the obese women. It is concluded that AT and SM are both significant sources of lactate release postabsorptively, and AT is at least as responsive to insulin as SM. The ability to increase lactate release in response to insulin is impaired in AT and SM in insulin-resistant obese women, involving defective insulin regulation of both tissue lactate metabolism and local blood flow. microdialysis; blood flow

To investigate the antilipolytic effect of insulin in skeletal muscle and adipose tissue in vivo, the rates of glycerol release from the two tissues were compared in 10 nonobese women during a two-step euglycemic hyper-insulinemic clamp, Tissue interstitial glycerol levels were determined by microdialysis, and tissue blood flow was assessed with the [sup.133]Xe clearance technique. Absolute rates of glycerol release were estimated according to Fick's principle. In both adipose tissue and muscle, glycerol levels decreased significantly already during the low insulin infusion rate. The fractional release of glycerol (difference between interstitial glycerol and arterialized venous plasma glycerol) was reduced by more than one-half in adipose tissue (P < 0.0001) in response to insulin, whereas it remained unaltered in skeletal muscle. Muscle blood flow rates increased by 60% (P < 0.02) during insulin infusion; in adipose tissue, blood flow rates did not change significantly in response to insulin. The basal rate of glycerol release from skeletal muscle amounted to ~15% of that from adipose tissue. After insulin infusion, the rate of adipose tissue glycerol release was markedly suppressed, whereas in skeletal muscle the rate of glycerol mobilization did not change significantly in response to insulin. It is concluded that insulin does not inhibit the rate of lipolysis in skeletal muscle of nonobese women. glycerol; microdialysis; blood flow

Research was conducted to characterize the beta-adrenoceptor subtypes that are involved in the in vivo regulation of lipolysis in muscle using the microdialysis method. Results indicate that the beta-2- adrenoceptor is the major adrenoceptor subtype that is vital for the regulation of blood flow in human skeletal muscle. Thus, some involvement of other beta-adrenoceptor subtypes in the regulation of muscle blood flow cannot be excluded.

Research was conducted to investigate concentrations of glycerol and lactate with microdialysis of adipose tissue and skeletal muscle at rest and during conditions that alter lipid and carbohydrate metabolism. Enzymatic fluorometric methods were utilized to measure dialysate glycerole and lactate concentrations. Results indicated that insulin inhibits lipid mobilization and activates lactate production in adipose tissue and skeletal muscle.

Insulin-dependent diabetes can re-occur in patients who receive a pancreas transplant even though they receive immunosuppressive drugs. This was demonstrated in two diabetic patients who received a pancreas transplant from a cadaver. Neither transplant was a good match. Both patients received cyclosporine, azathioprine and prednisolone to suppress graft rejection. However, the autoimmune process believed to underly type 1 diabetes continued to destroy the beta cells in the transplanted pancreas. Both patients had to resume insulin injections.