An immune origin of type 2 diabetes?

Kolb, Hubert; Mandrup-Poulsen, Thomas

doi:10.1007/s00125-005-1764-9

Cited by 379 publications

(302 citation statements)

References 233 publications

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“…Since subclinical inflammation increases the risk of cardiovascular disease, disability, neurodegenerative disorders and cancers [20][21][22][23][24], it is important to identify efficient ways to modulate low-grade immune activation. Lifestylebased interventions are one option as they have been proved to exert anti-inflammatory effects in many studies [17,32].…”

Section: Discussionmentioning

confidence: 99%

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Anti-inflammatory effect of lifestyle changes in the Finnish Diabetes Prevention Study

Peltonen²,

et al. 2009

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Aims/hypothesis Subclinical inflammation confers an increased risk of type 2 diabetes, cardiovascular disease, neurodegenerative disorders and other age-related chronic diseases. Physical activity and diet can attenuate systemic immune activation, but it is not known which individual components of a comprehensive lifestyle intervention are most effective in targeting subclinical inflammation.Methods We used data from the baseline examination and the 1 year follow-up of a subsample of 406 of 522 participants of the Finnish Diabetes Prevention Study (DPS) to estimate the effect of individual components of lifestyle intervention on C-reactive protein (CRP) and IL-6 levels, which represent the best characterised proinflammatory risk factors for type 2 diabetes. Changes in metabolic markers, dietary patterns and exercise were analysed to Diabetologia (2009) determine which were most strongly associated with the anti-inflammatory effect of lifestyle changes. Results Lifestyle intervention reduced circulating levels of CRP (p<0.001) and . Increases in fibre intake and moderate to vigorous leisure time physical activity (LTPA), but not total LTPA, predicted decreases in CRP and/or IL-6 and remained associated even after adjustment for baseline BMI or changes in BMI during the first year of the study. Changes in carbohydrate or fat intake were either weakly or not linked to reductions in CRP and IL-6. Conclusions/interpretation The present study assessed the individual effects of dietary and physical activity measures on low-grade inflammation in individuals at high cardiometabolic risk. Our results underline the importance of moderate to vigorous LTPA and a diet rich in natural fibre, and this should be emphasised in lifestyle recommendations.

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Section: Discussionmentioning

confidence: 99%

“…In addition to type 2 diabetes, subclinical inflammation is also a risk factor for cardiovascular disease, neurodegenerative disorders, depression and some cancers [20][21][22][23][24], which means that the identification of the mechanisms that modulate and attenuate systemic immune activation has widespread implications.…”

Section: Introductionmentioning

confidence: 99%

Anti-inflammatory effect of lifestyle changes in the Finnish Diabetes Prevention Study

Peltonen²,

et al. 2009

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“…In this review we expand the concept of an immune or inflammatory origin of type 2 diabetes that has been discussed previously [4]. We discuss whether the changes of lifestyle in past decades have promoted inflammatory processes, thereby causing increased insulin demands and beta cell death.…”

Section: Introductionmentioning

confidence: 88%

The global diabetes epidemic as a consequence of lifestyle-induced low-grade inflammation

Kolb¹,

2009

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The recent major increase in the global incidence of type 2 diabetes suggests that most cases of this disease are caused by changes in environment and lifestyle. All major risk factors for type 2 diabetes (overnutrition, low dietary fibre, sedentary lifestyle, sleep deprivation and depression) have been found to induce local or systemic low-grade inflammation that is usually transient or milder in individuals not at risk for type 2 diabetes. By contrast, inflammatory responses to lifestyle factors are more pronounced and prolonged in individuals at risk of type 2 diabetes and appear to occur also in the pancreatic islets. Chronic low-grade inflammation will eventually lead to overt diabetes if counter-regulatory circuits to inflammation and metabolic stress are compromised because of a genetic and/or epigenetic predisposition. Hence, it is not the lifestyle change per se but a deficient counter-regulatory response in predisposed individuals which is crucial to disease pathogenesis. Novel approaches of intervention may target these deficient defence mechanisms.

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“…Activation of innate immunity and complex changes in inflammatory patterns have been found to play a significant role in the pathogenesis of type 2 diabetes and insulin resistance [32], and a recent hypothesis on the pivotal role of inflammatory cytokines and oxidative/nitrosative stress in the pathogenesis of depression has recieved much attention [33]. Whether or not inflammatory response and the resulting oxidative damage in diabetes is primary or reactive is not clear, but its significant association with both insulin resistance and beta cell dysfunction, as well as with many different co-morbidities (atherosclerosis, obesity, depression), definitively suggests that the activation of innate immunity should be regarded as more than just an epiphenomenon.…”

Section: Introductionmentioning

confidence: 99%

Does treatment of subsyndromal depression improve depression and diabetes related outcomes: protocol for a randomised controlled comparison of psycho-education, physical exercise and treatment as usual

Pibernik-Okanović

Ajduković

Lovrenčić

et al. 2011

Trials

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BackgroundThe prevalence of mood difficulties in persons with diabetes is approximately twice that in the general population, affecting the health outcomes and patients' quality of life in an undesirable way. Although subsyndromal depression is an important predictor of a more serious clinical depression, it is often overlooked. This study aims to compare the effects of two non-pharmacological interventions for subsyndromal depression, psychoeducation and physical exercise, with diabetes treatment as usual on mood- and diabetes-related outcomes.Methods and DesignType 2 diabetic patients aged 18-65 yrs. who report mood difficulties and the related need for help in a mail survey will be potential participants. After giving informed consent, they will be randomly assigned to one of the three groups (psychoeducation, physical activity, treatment as usual). Depressive symptoms, diabetes distress, health-related quality of life and diabetes self-care activities will be assessed at baseline, at 6 weeks, 6 months and 12 months. A structured clinical interview for DSM-IV Axis I Disorders (SCID-I) will be performed at baseline and at one-year follow-up in order to determine the clinical significance of the patients' depressive symptoms. Disease-related data will be collected from patients' files and from additional physical examinations and laboratory tests.The two interventions will be comparable in terms of format (small group work), duration (six sessions) and approach (interactive learning; supporting the participants' active roles). The group treated as usual will be informed about their screening results and about the importance of treating depression. They will be provided with brief re-education on diabetes and written self-help instructions to cope with mood difficulties.Primary outcomes will be depressive symptoms. Secondary outcomes will be glycaemic control, diabetes-related distress, self-management of diabetes and health-related quality of life. Tertiary outcomes will be biochemical markers reflecting common pathophysiological processes of insulin resistance, inflammation and oxidative damage that are assumed to be intertwined in both diabetes and depression. The mixed-effect linear model will be used to compare the outcome variables.Power analysis has indicated that the two intervention groups and the control group should comprise 59 patients to enable detection of clinically meaningful differences in depressive symptoms with a power of 80% and alpha = 0.05. Outcomes will be analysed on an intention-to-treat basis.Trial RegistrationISRCTN: ISRCTN05673017

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An immune origin of type 2 diabetes?

Cited by 379 publications

References 233 publications

Anti-inflammatory effect of lifestyle changes in the Finnish Diabetes Prevention Study

Anti-inflammatory effect of lifestyle changes in the Finnish Diabetes Prevention Study

The global diabetes epidemic as a consequence of lifestyle-induced low-grade inflammation

Does treatment of subsyndromal depression improve depression and diabetes related outcomes: protocol for a randomised controlled comparison of psycho-education, physical exercise and treatment as usual

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