Adiponectin, secreted mainly by mature adipocytes, is a protein with insulin-sensitising and anti-atherogenic effects. Human adiponectin is encoded by the ADIPOQ gene on the chromosomal locus 3q27. Variations in ADIPOQ are associated with obesity, type 2 diabetes (T2DM) and related phenotypes in several populations. Our aim was to study the association of the ADIPOQ variations with body weight, serum adiponectin concentrations and conversion to T2DM in overweight subjects with impaired glucose tolerance. Moreover, we investigated whether ADIPOQ gene variants modify the effect of lifestyle changes on these traits.
Participants in the Finnish Diabetes Prevention Study were randomly assigned to a lifestyle intervention group or a control group. Those whose DNA was available (n = 507) were genotyped for ten ADIPOQ single nucleotide polymorphisms (SNPs). Associations between SNPs and baseline body weight and serum adiponectin concentrations were analysed using the univariate analysis of variance. The 4-year longitudinal weight data were analysed using linear mixed models analysis and the change in serum adiponectin from baseline to year four was analysed using Kruskal-Wallis test. In addition, the association of SNPs with the risk of developing T2DM during the follow-up of 0-11 (mean 6.34) years was analysed by Cox regression analysis.
rs266729, rs16861205, rs1501299, rs3821799 and rs6773957 associated significantly (p
Cites: Circulation. 1999 Dec 21-28;100(25):2473-610604883
The association of the Pro12Ala polymorphism of the PPAR-gamma2 gene with the incidence of type 2 diabetes was investigated in 522 subjects with impaired glucose tolerance (IGT) participating in the Finnish Diabetes Prevention Study. Subjects were randomized to either an intensive diet and exercise group or a control group. By 3 years of intervention, the odds ratio of the development of type 2 diabetes for subjects with the Ala12 allele was 2.11-fold compared with that for subjects with the Pro12Pro genotype (95% CI 1.20-3.72). The risk for type 2 diabetes increased also in subjects who gained weight or belonged to the control group. In the intervention group, subjects with the Ala12Ala genotype lost more weight during the follow-up than subjects with other genotypes (Pro12Pro vs. Ala12Ala P = 0.043), and none of subjects with the Ala12Ala genotype developed type 2 diabetes in this group. In conclusion, the Ala12 allele may predispose to the development of type 2 diabetes in obese subjects with IGT. However, beneficial changes in diet, increases in physical activity, and weight loss may reverse, to some extent, the diabetogenic impact of the Ala12 allele, possibly due to an improved insulin sensitivity.
To study screening of high-risk individuals as part of a national diabetes prevention programme in primary health care settings in Finland between 2003 and 2007, and evaluate the cardiometabolic risk profile of persons identified for intervention.
High-risk individuals were identified by the Finnish Diabetes Risk Score (FINDRISC), history of impaired fasting glucose (IFG), impaired glucose tolerance (IGT), cardiovascular disease (CVD), or gestational diabetes. Participants subsequently underwent an oral glucose tolerance test. CVD morbidity risk was estimated by the Framingham Study Risk Equation and CVD mortality risk by the Systematic Coronary Risk Evaluation Formula (SCORE).
A high-risk cohort of 10,149 (of whom 30.3% men) was identified (mean age 54.7 for men, 53.0 for women). Altogether 18.8% of men and 11.5% of women had screen-detected diabetes. In total 68.1% of men and 49.4% of women had abnormal glucose tolerance (IFG, IGT or screen-detected diabetes). Furthermore, 43.2% and 41.5% of men, and 13.3% and 11.3% of women, respectively, had a high predicted risk of CVD morbidity or mortality.
Prevalence of dysglycemia including undiagnosed diabetes and the predicted risk for CVD was alarmly high in the identified high-risk cohort, particularly in men.
The purpose of this study was to assess whether changes in self-rated physical activity and diet during a type 2 diabetes (T2D) prevention program were associated with changes in estimated 10-year risk for cardiovascular disease (CVD) events and mortality in people at high risk for T2D.
Individuals were identified and offered lifestyle counseling as part of the Finnish diabetes prevention program. Ten-year risk for estimated CVD events and mortality were calculated with Framingham Risk Score (FRS) and Systematic Coronary Risk Evaluation (SCORE) formula. FRS was available for 774 men and 1474 women and SCORE for 961 men and 1766 women.
During the one-year follow-up, 9.6% of the men reported both an increase in physical activity and improved dietary pattern, 4.1% an increase in physical activity, 39.3% an increase in improved dietary pattern, while 47.0% reported no lifestyle changes. Corresponding numbers for women were 14.2%, 3.8%, 39.2% and 42.7%. Estimated 10-year risk for CVD events decreased 3.5% in men and 1.5% in women reporting an increase in physical activity and improvement in diet, compared to an increase of 0.15% in men (p
We studied cognition in the Finnish Diabetes Prevention Study (DPS), a trial of lifestyle intervention that prevented diabetes in persons with impaired glucose tolerance. Cognition was similar in the randomization arms 9 years after the intervention in 364 participants, suggesting that the intervention did not benefit cognition.
Intensive lifestyle intervention significantly reduced diabetes incidence among the participants in the Finnish Diabetes Prevention Study. We investigated whether and to what extent risk factors for type 2 diabetes and other baseline characteristics of the study participants modified the effectiveness of the lifestyle intervention.
Overweight, middle-aged volunteers with impaired glucose tolerance were randomly assigned to intensive lifestyle intervention (n = 265) or to a control group (n = 257) for a median of 4 years. Diabetes status was ascertained annually with repeated oral glucose tolerance testing. Incidence rates of diabetes and hazard ratios (HRs) comparing the intervention group with the control group were calculated by sex and baseline tertiles of age, BMI, waist circumference, plasma glucose concentration at fasting and 2 h after a glucose load, fasting serum insulin and insulin resistance index, and categories of composite baseline Finnish Diabetes Risk Score (FINDRISC). Interactions between the intervention assignment and baseline risk factors on diabetes risk were analyzed.
The intervention was most effective among the oldest individuals (HRs 0.77, 0.49, and 0.36 by increasing age tertiles, respectively; P(interaction) = 0.0130) and those with a high baseline FINDRISC (HRs 1.09, 0.84, 0.34, and 0.22 by increasing risk score category, respectively; P(interaction) = 0.0400). The effect of the intervention on diabetes risk was not modified by other baseline characteristics or risk factors.
The FINDRISC may be useful in identifying high-risk groups most likely to benefit from intensive lifestyle intervention to prevent type 2 diabetes.
Type 2 diabetes is linked with cognitive dysfunction and dementia in epidemiological studies, but these observations are limited by lack of data on the exact timing of diabetes onset. We investigated diabetes, dysglycaemia, and cognition in the Finnish Diabetes Prevention Study, in which the timing and duration of diabetes are well documented.
The Finnish Diabetes Prevention Study comprised middle-aged, overweight participants with impaired glucose tolerance but no diabetes at baseline (n?=?522), randomized to lifestyle intervention or a control group. After an intervention period (mean duration 4 years) and follow-up (additional 9 years), cognitive assessment with the CERAD test battery and Trail Making Test A (TMT) was executed twice within a 2-year interval. Of the 364 (70%) participants with cognitive assessments, 171 (47%) had developed diabetes.
Cognitive function did not differ between those who developed diabetes and those who did not. Lower mean 2-h glucose at an oral glucose tolerance test (OGTT) and HbA1C during the intervention period predicted better performance in the TMT (p?=?0.012 and 0.024, respectively). Those without diabetes or with short duration of diabetes improved in CERAD total score between the two assessments (p?=?0.001) whereas those with long duration of diabetes did not (p?=?0.844).
To examine whether depressive symptoms are associated with the effectiveness of lifestyle counseling on cardio-metabolic risk profile and glucose homeostasis during one-year follow-up in individuals at high risk for type 2 diabetes (T2D).
A total of 10,149 individuals took part in the implementation project of the national diabetes prevention program (FIN-D2D) conducted in primary health care setting in Finland. At baseline, altogether 2798 non-diabetic individuals participated in the one-year follow-up, and 2275 of them had at least one group or individual counseling visit.
4.0% of the individuals (n=78) had depressive symptoms, while 96.0% (n=1889) were free of depressive symptoms at baseline. Individuals who had depressive symptoms had higher body mass index and waist circumference at baseline than individuals without depressive symptoms. In terms of changes in cardio-metabolic risk profile and glucose homeostasis the effectiveness of lifestyle counseling was parallel between individuals with and without depressive symptoms during the one-year follow-up.
Effectiveness of lifestyle counseling did not differ between individuals with and without depressive symptoms. Individuals with depressive symptoms should not be excluded from lifestyle intervention programs.
We used data from the Finnish Diabetes Prevention Study to analyze the effectiveness of lifestyle intervention according to educational attainment. The effect of intervention on lifestyle changes and diabetes incidence was independent of education. The prevention of type 2 diabetes by lifestyle intervention is effective regardless of participants' educational attainment.