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Objective: Charcot foot is a serious complication of diabetes, with degeneration of the bones and joints in the foot and ankle. It is unknown whether patients with diabetes with a Charcot foot have an increased risk of osteoporosis and fractures. The aim of this study was to investigate whether patients with diabetes with a Charcot foot have an increased risk of fracture and/or osteoporosis compared with patients with diabetes without Charcot foot., Research Design and Methods: A Danish register-based, nationwide population-based matched cohort study was conducted. During 1995-2018, we identified 1,602 patients with diabetes with Charcot foot and matched them on sex and date of diagnosis of diabetes with 16,296 patients with diabetes without Charcot foot. We used logistic regression to estimate odds ratios (ORs) with 95% CIs for fracture and osteoporosis. Information about exposure, outcome, and comorbidities was retrieved from the Danish National Patient Register., Results: Diabetes patients with Charcot foot had higher risk of fractures compared with those without Charcot foot (i.e., ORs for any fracture, lower-leg fracture, foot fracture, and osteoporotic fracture were 1.8 [95% CI 1.6-2.0], 2.4 [2.0-2.8], 2.9 [2.6-3.3], and 1.3 [1.1-1.4], respectively). Furthermore, patients with diabetes with Charcot foot had higher risk of osteoporosis compared with the patients without Charcot foot, with an OR of 1.3 (95% CI 1.1-1.5)., Conclusions: Patients with diabetes with a Charcot foot have an increased risk of fractures and osteoporosis compared with patients with diabetes without a Charcot foot., (© 2021 by the American Diabetes Association.)

Objective: We investigated the processes underlying glycemic deterioration in type 2 diabetes (T2D)., Research Design and Methods: A total of 732 recently diagnosed patients with T2D from the Innovative Medicines Initiative Diabetes Research on Patient Stratification (IMI DIRECT) study were extensively phenotyped over 3 years, including measures of insulin sensitivity (OGIS), β-cell glucose sensitivity (GS), and insulin clearance (CLIm) from mixed meal tests, liver enzymes, lipid profiles, and baseline regional fat from MRI. The associations between the longitudinal metabolic patterns and HbA 1c deterioration, adjusted for changes in BMI and in diabetes medications, were assessed via stepwise multivariable linear and logistic regression., Results: Faster HbA 1c progression was independently associated with faster deterioration of OGIS and GS and increasing CLIm; visceral or liver fat, HDL-cholesterol, and triglycerides had further independent, though weaker, roles ( R 2 = 0.38). A subgroup of patients with a markedly higher progression rate (fast progressors) was clearly distinguishable considering these variables only (discrimination capacity from area under the receiver operating characteristic = 0.94). The proportion of fast progressors was reduced from 56% to 8-10% in subgroups in which only one trait among OGIS, GS, and CLIm was relatively stable (odds ratios 0.07-0.09). T2D polygenic risk score and baseline pancreatic fat, glucagon-like peptide 1, glucagon, diet, and physical activity did not show an independent role., Conclusions: Deteriorating insulin sensitivity and β-cell function, increasing insulin clearance, high visceral or liver fat, and worsening of the lipid profile are the crucial factors mediating glycemic deterioration of patients with T2D in the initial phase of the disease. Stabilization of a single trait among insulin sensitivity, β-cell function, and insulin clearance may be relevant to prevent progression., (© 2020 by the American Diabetes Association.)