Stefan L C Geijselaers1, Simone J S Sep2, Miranda T Schram2, Martin P J van Boxtel3, Ronald M A Henry2, Frans R J Verhey3, Abraham A Kroon2, Nicolaas C Schaper4, Pieter C Dagnelie5, Carla J H van der Kallen2, Coen D A Stehouwer2, Geert Jan Biessels6. 1. Department of Internal Medicine, Maastricht University Medical Center +, Maastricht, the Netherlands; CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, the Netherlands; Department of Neurology, Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, the Netherlands. Electronic address: stefan.geijselaers@gmail.com. 2. Department of Internal Medicine, Maastricht University Medical Center +, Maastricht, the Netherlands; CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, the Netherlands. 3. Department of Psychiatry and Neuropsychology and MHeNS School for Mental Health and Neuroscience, Maastricht University Medical Center +, Maastricht, the Netherlands. 4. Department of Internal Medicine, Maastricht University Medical Center +, Maastricht, the Netherlands; CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, the Netherlands; CAPHRI School for Public Health and Primary Care, Maastricht University, Maastricht, the Netherlands. 5. CARIM School for Cardiovascular Diseases, Maastricht University, Maastricht, the Netherlands; CAPHRI School for Public Health and Primary Care, Maastricht University, Maastricht, the Netherlands; Department of Epidemiology, Maastricht University, Maastricht, the Netherlands. 6. Department of Neurology, Brain Center Rudolf Magnus, University Medical Center Utrecht, Utrecht, the Netherlands.
Abstract
AIMS: Type 2 diabetes, hyperinsulinemia, and insulin resistance are associated with cognitive impairment. Experimental studies indicate that insulin signaling in the brain is related to cognitive performance. Here we evaluated whether insulin-related variables contribute to the variance in cognitive performance among individuals with type 2 diabetes. METHODS: A total of 806 individuals with type 2 diabetes (mean age 62±8years, HbA1c 6.9±1.1%) completed a neuropsychological test battery. Insulin-related variables evaluated were: fasting plasma insulin, C-peptide, and the Homeostasis Model Assessment (HOMA2-IR; in individuals without insulin treatment; n=641). The unadjusted coefficient of determination (R2), obtained from multiple linear regression analyses, was used to estimate the proportion of variance in cognition explained by insulin-related variables. RESULTS: Sex, age, and educational level together explained 18.0% (R2) of the variance in memory function, 26.5% in information processing speed, and 22.8% in executive function and attention. Fasting insulin, C-peptide, or HOMA2-IR did not increase the explained variance (maximum ΔR2 0.3%, P≥0.14). Similar results were obtained when insulin-related variables were added to models that additionally included glycemic control, cardiovascular risk factors, and depression. CONCLUSIONS: Our results show that measures of peripheral insulin resistance are unrelated to cognitive performance among individuals with adequately controlled type 2 diabetes.
AIMS: Type 2 diabetes, hyperinsulinemia, and insulin resistance are associated with cognitive impairment. Experimental studies indicate that insulin signaling in the brain is related to cognitive performance. Here we evaluated whether insulin-related variables contribute to the variance in cognitive performance among individuals with type 2 diabetes. METHODS: A total of 806 individuals with type 2 diabetes (mean age 62±8years, HbA1c 6.9±1.1%) completed a neuropsychological test battery. Insulin-related variables evaluated were: fasting plasma insulin, C-peptide, and the Homeostasis Model Assessment (HOMA2-IR; in individuals without insulin treatment; n=641). The unadjusted coefficient of determination (R2), obtained from multiple linear regression analyses, was used to estimate the proportion of variance in cognition explained by insulin-related variables. RESULTS: Sex, age, and educational level together explained 18.0% (R2) of the variance in memory function, 26.5% in information processing speed, and 22.8% in executive function and attention. Fasting insulin, C-peptide, or HOMA2-IR did not increase the explained variance (maximum ΔR2 0.3%, P≥0.14). Similar results were obtained when insulin-related variables were added to models that additionally included glycemic control, cardiovascular risk factors, and depression. CONCLUSIONS: Our results show that measures of peripheral insulin resistance are unrelated to cognitive performance among individuals with adequately controlled type 2 diabetes.
Authors: Jolien Janssen; Esther van den Berg; Bernard Zinman; Mark A Espeland; Stefan L C Geijselaers; Michaela Mattheus; Odd Erik Johansen; Geert Jan Biessels Journal: Diabetes Care Date: 2019-01 Impact factor: 19.112