Abstract 021: C-reactive Protein Partially Mediates The Inverse Association Between Coffee Consumption And Risk Of Type 2 Diabetes: Findings From The UK Biobank And The Rotterdam Studies

Circulation ◽  
2021 ◽  
Vol 143 (Suppl_1) ◽  
Author(s):  
Carolina Ochoa-Rosales ◽  
Niels van der Schaft ◽  
Kim V Braun ◽  
Frederick Ho ◽  
Fanny Petermann ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Coffee Consumption ◽  
Inverse Association ◽  
Statistical Regression ◽  
Uk Biobank ◽  
C Reactive Protein ◽  
Coffee Intake ◽  
Reactive Protein ◽  
The Uk

Background: Coffee intake has been linked to lower type 2 diabetes (T2D) risk. We hypothesized this may be mediated by coffee’s effects on inflammation. Methods: Using participants from the UK Biobank (UKB n=145370) and Rotterdam Study (RS n=7172) cohorts, we studied associations of coffee intake with incident T2D; longitudinally measured insulin resistance (HOMA IR); serum levels of inflammation markers; and the mediating role of inflammation. Statistical regression models were adjusted for sociodemographic, lifestyle and health factors. Results: The median follow up was 7 (UKB) and 9 (RS) years. An increase of one coffee cup/day was associated with 4-6% lower T2D risk (RS HR=0.94 [95% CI 0.90; 0.98]; UKB HR=0.96 [0.94; 0.98]); lower HOMA IR (RS β=-0.017 [-0.024; -0.010]); with lower C reactive protein (CRP) and higher adiponectin (Figure1). Consumers of filtered coffee had the lowest T2D risk (UKB HR=0.88 [0.83; 0.93]). CRP levels mediated 9.6% (UKB) and 3.4% (RS) of the total effect of coffee on T2D (Figure 1). Conclusions: We suggest that coffee’s beneficial effects on lower T2D risk are partially mediated by improvements in systemic inflammation.Figure 1. a CRP and a adiponectin refer to the effect of coffee intake on CRP and adiponectin levels. a CRP RS : β=-0.014 (-0.022; -0.005); UKBB a CRP UKB : β=-0.011 (-0.012; -0.009) and RS a adiponectin : β=0.025 (0.007; 0.042). b CRP and b adiponectin refer to the effect of coffee related levels in CRP and adiponectin on incident T2D, independent of coffee. RS b CRP : HR=1.17 (1.04; 1.31); UKB b CRP : HR=1.45 (1.37; 1.54); and b adiponectin : HR=0.58 (0.32; 0.83). c′ refers to coffee’ effect on T2D going directly or via others mediators. UKB c′ independent of CRP : HR=0.96 (0.94; 0.99); RS c′ independent of CRP : HR=0.94 (0.90; 0.99); and RS c′ independent of CRP+adiponectin : HR=0.90 (0.80; 1.01). Coffee related changes in CRP may partially explain the beneficial link between coffee and T2D, mediating a 3.4% (0.6; 4.8, RS) and 9.6% (5.7; 24.4, UKB). Evidence of mediation was also found for adiponectin.

scholarly journals C-Reactive Protein Partially Mediates the Inverse Association Between Coffee Consumption and Risk of Type 2 Diabetes: The UK Biobank and the Rotterdam Study Cohorts

2021 ◽  
Vol 5 (Supplement_2) ◽  
pp. 1070-1070
Author(s):  
Carolina Ochoa-Rosales ◽  
Niels van der Schaft ◽  
Kim Braun ◽  
Frederick Ho ◽  
Fanny Petermann ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Systemic Inflammation ◽  
Coffee Consumption ◽  
Uk Biobank ◽  
Rotterdam Study ◽  
C Reactive Protein ◽  
Coffee Intake ◽  
Reactive Protein ◽  
Filtered Coffee

Abstract Objectives Given its popularity, there is an increasing interest in the study of coffee intake and its effect on health. Previous studies linked coffee consumption to lower type 2 diabetes (T2D) risk. However, potential underlying mechanisms remain unclear. We hypothesized that coffee's effects on systemic inflammation may play a role. We studied cross sectional and longitudinal associations of habitual coffee consumption with T2D risk and inflammation. Methods Participants from UK Biobank (UKB, n = 145,370) and Rotterdam Study (RS, n = 7172) cohorts were included. Coffee intake data were collected through self-administrated food frequency questionnaire or during home interviews. We studied associations of coffee intake with incident T2D using cox proportional hazard models; with longitudinally measured insulin resistance (HOMA IR) through linear mixed effect models; with serum baseline levels of inflammation markers using linear regressions; and the role of inflammation in coffee-T2D associations using mediation analysis. Models were adjusted for sociodemographic, lifestyle and health factors. Results were respectively expressed as hazard ratio (HR); β log transformed HOMA IR level; β log transformed ug/mL; and percentage mediated; and 95% confidence interval [95% CI]. Results UKB participants were 58% female and 55.2 years in average; RS were 59.7% female and 65.1 years. The median follow up was 7 (UKB) and 9 (RS) years. The modal coffee consumption was 0.5–2 cups/day (UKB) and 3–4 cups/day (RS). An increase of one coffee cup/day was associated with 4–6% lower T2D risk (RS HR 0.94 [95% CI 0.90; 0.98]; UKB HR 0.96 [0.94; 0.98]); lower HOMA IR (RS β −0.017 [−0.024; −0.010]); lower C reactive protein (CRP, RS β −0.014 [−0.022; −0.005]; UKBB β −0.011 [−0.012; −0.009] and higher adiponectin (RS β 0.025 [0.007; 0.042]. About coffee types, habitual consumers of filtered coffee had the lowest T2D risk (UKB HR 0.88 [0.83; 0.93]), compared to decaffeinated or instantaneous coffee. CRP levels mediated 9.6% (UKB) and 3.4% (RS) of the total effect of coffee on T2D. Adiponectin also showed evidence for mediation. Conclusions Coffee's beneficial effects on lower T2D risk may be partially mediated by improvements in systemic inflammation. Among coffee drinkers, filtered coffee may be of preference. Funding Sources Partially funded by the Institute for Scientific Information on Coffee.

scholarly journals Association between fasting insulin and C-reactive protein among adults without diabetes using a two-part model: NHANES 2005–2010

2021 ◽  
Vol 13 (1) ◽  
Author(s):  
Amanda L. Missel ◽  
Laura R. Saslow ◽  
Dina H. Griauzde ◽  
Donna Marvicsin ◽  
Ananda Sen ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Waist Circumference ◽  
Low Grade ◽  
Fasting Insulin ◽  
C Reactive Protein ◽  
Glucose Levels ◽  
Reactive Protein ◽  
Part Model

Abstract Introduction Chronic inflammation is associated with the development, progression and long-term complications of type 2 diabetes. Hyperglycemia is associated with chronic low-grade inflammation, and thus has become the focus of many screening and treatment recommendations. We hypothesize that insulin may also be associated with inflammation and may be an additional factor to consider in screening and treatment. Methods This study used National Health and Nutrition Examination Survey data from 2005 to 2010 to analyze the association between fasting insulin and C-reactive protein (CRP). A two-part model was used due to the high number of values reported as 0.1 mg/L. Two models were analyzed, both with and without the addition of waist circumference to other covariates in the model. Results The final sample included 4527 adults with a mean age of 43.31 years. In the first model, higher fasting insulin was associated with increased odds of CRP > 0.1 mg/L (OR = 1.02, p < .001) and with higher CRP (β = 0.03, p < .001). In the adjusted model, including waist circumference as a covariate, higher fasting insulin was not associated with CRP > 0.1 mg/L (OR = 1.00, p = .307) but the association between higher fasting insulin and higher continuous CRP remained significant (β = 0.01, p = .012). Conclusion This study found that higher fasting insulin is associated with higher CRP. These results suggest that treatment approaches that simultaneously decrease insulin levels as well as glucose levels may provide additive anti-inflammatory effects, and therefore may improve long-term outcomes for adults with type 2 diabetes.

C-reactive protein: a marker or a player?

2007 ◽  
Vol 113 (2) ◽  
pp. 79-81 ◽  
Author(s):  
Thomas Nyström
Keyword(s):  
Type 2 Diabetes ◽  
Cardiovascular Events ◽  
Protein A ◽  
Low Grade ◽  
Phase Reaction ◽  
Clinical Markers ◽  
C Reactive Protein ◽  
Reactive Protein ◽  
Hs Crp

It has been suggested that Type 2 diabetes may, in part, be precipitated or accelerated by an acute-phase reaction as part of the innate immune response, in which large amounts of cytokines are released from adipose tissue, creating a low-grade inflammatory milieu. There is also firm evidence that atherosclerosis is an immune-mediated inflammatory disease. Therefore it is reasonable to imply that low-grade inflammation is an important pathogenetic factor in atherosclerosis and cardiovascular events in patients with Type 2 diabetes. Over the last few years, there have been a lot of promising clinical markers proposed to link inflammation and atherosclerosis. Of these markers, hs-CRP (high-sensitivity C-reactive protein) might be a prognostic marker for further cardiovascular events, although this has been refuted recently. In this issue of Clinical Science, Castoldi and co-workers have demonstrated that, in patients with Type 2 diabetes categorized into low (<1.0 mg/l), medium (1.0–3.0 mg/l) and high (>3.0 mg/l) hs-CRP groups, serum levels of hs-CRP correlated with lipopolysaccharide-stimulated release of interleukin-1β and interleukin-6 in whole blood. This finding may indicate that low-grade inflammatory activity might influence cytokine production in these patients.

scholarly journals Prospective Relation of C-Reactive Protein With Type 2 Diabetes: Response to Han et al.

Diabetes Care ◽  
2003 ◽  
Vol 26 (5) ◽  
pp. 1656-1657 ◽  
Author(s):  
M. B. Snijder ◽  
J. M. Dekker ◽  
M. Visser ◽  
C. D.A. Stehouwer ◽  
J. S. Yudkin ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
C Reactive Protein ◽  
Reactive Protein

Abstract P137: Aerobic, Resistance or Combination Exercise Training does not Reduce C-Reactive Protein Levels in Individuals with Type 2 Diabetes

Circulation ◽  
2012 ◽  
Vol 125 (suppl_10) ◽  
Author(s):  
Damon L Swift ◽  
Neil M Johannsen ◽  
Conrad P Earnest ◽  
Steven N Blair ◽  
Timothy S Church
Keyword(s):  
Type 2 Diabetes ◽  
Exercise Training ◽  
Aerobic Exercise ◽  
Fat Mass ◽  
Fasting Glucose ◽  
Aerobic Exercise Training ◽  
C Reactive Protein ◽  
Protein Levels ◽  
Reactive Protein

Introduction: Type 2 diabetes is associated with elevated C-reactive protein levels (CRP), which is an independent risk factor for cardiovascular disease. Aerobic exercise training especially with weight/adiposity reduction has been shown to improve CRP, however few studies have evaluated the effect of other exercise training modalities (aerobic, resistance or combination training) on CRP in individuals with type 2 diabetes. Hypothesis: We hypothesize that combination training will improve CRP to a greater extent than other modalities of exercise training, and change in CRP levels will be associated with changes in weight and adiposity. Methods: The present study is a secondary analysis of the Health Benefits of Aerobic and Resistance Training in Individuals with Type 2 Diabetes (HART-D) study. Participants (n=204) were randomized to aerobic exercise (aerobic), resistance exercise (resistance) or a combination of both (combination) for nine months. Results: Baseline CRP was correlated with fat mass, waist circumference, BMI, and inversely correlated with VO2 peak (p<0.05). CRP was not reduced in the aerobic (0.16 mg•L-1, 95% CI: -1.0, 1.3), resistance (-0.03 mg•L-1, 95% CI: -1.1, 1.0) or combination (-0.49 mg•L-1, 95% CI: -1.5 to 0.6) groups compared to control (0.35 mg•L-1, 95% CI: -1.0, 1.7). Change in CRP was associated with change in fasting glucose (r=0.20, p= 0.009), glycated hemoglobin (HbA1C) (r=0.21 p=0.005), and fat mass (r=0.19, p=0.016), but not change in fitness or weight (p > 0.05). Conclusions: In conclusion, aerobic, resistance or a combination of both did not reduce CRP levels in individuals with type 2 diabetes. However, exercise related improvements in HbA1C, fasting glucose, and fat mass were associated with reductions in CRP.

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