Nutrition and Cytokine Action

Grimble, R. F.

doi:10.1079/nrr19900012

Cited by 97 publications

(45 citation statements)

References 104 publications

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“…6,8 -10,12 In a previous interventional study, the synthesis of proinflammatory cytokines by peripheral monocytes (TNF-␣, IL-1) was suppressed by dietary fish oil supplementation, 37 suggesting an effect of dietary fat on cytokine production. 38 Another (speculative at this time) mechanism would be a generally enhanced adipose tissue-derived cytokine expression (TNF-␣, IL-6). Accordingly, weight loss was associated with a decrease in CRP in the Women's Healthy Lifestyle Project (E. Meilahn, personal communication, 1996), also supporting an association of body fat and chronic inflammation.…”

Section: Festa Et Al Inflammation and Insulin Resistancementioning

confidence: 99%

Chronic Subclinical Inflammation as Part of the Insulin Resistance Syndrome

Festa

D’Agostino²,

Howard³

et al. 2000

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Background-Inflammation has been suggested as a risk factor for the development of atherosclerosis. Recently, some components of the insulin resistance syndrome (IRS) have been related to inflammatory markers. We hypothesized that insulin insensitivity, as directly measured, may be associated with inflammation in nondiabetic subjects. Methods and Results-We studied the relation of C-reactive protein (CRP), fibrinogen, and white cell count to components of IRS in the nondiabetic population of the Insulin Resistance Atherosclerosis Study (IRAS) (nϭ1008; age, 40 to 69 years; 33% with impaired glucose tolerance), a multicenter, population-based study. None of the subjects had clinical coronary artery disease. Insulin sensitivity (S I ) was measured by a frequently sampled intravenous glucose tolerance test, and CRP was measured by a highly sensitive competitive immunoassay. All 3 inflammatory markers were correlated with several components of the IRS. Strong associations were found between CRP and measures of body fat (body mass index, waist circumference), S I , and fasting insulin and proinsulin (all correlation coefficients Ͼ0.3, PϽ0.0001). The associations were consistent among the 3 ethnic groups of the IRAS. There was a linear increase in CRP levels with an increase in the number of metabolic disorders. Body mass index, systolic blood pressure, and S I were related to CRP levels in a multivariate linear regression model. Conclusions-We suggest that chronic subclinical inflammation is part of IRS. CRP, a predictor of cardiovascular events in previous reports, was independently related to S I . These findings suggest potential benefits of anti-inflammatory or insulin-sensitizing treatment strategies in healthy individuals with features of IRS. (Circulation. 2000;102:42-47.)

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Section: Festa Et Al Inflammation and Insulin Resistancementioning

confidence: 99%

Chronic Subclinical Inflammation as Part of the Insulin Resistance Syndrome

Festa

D’Agostino²,

Howard³

et al. 2000

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“…There are a number of ways in which nutrition can affect cytokine responses which are of relevance to Type II diabetes, for example, the effect of dietary fat on cytokine production [58]. Synthesis of proinflammatory cytokines by peripheral blood monocytes is suppressed by n-3 fatty acid supplementation (fish oil) in normal volunteers [59]; this supports the theory that a diet rich in n-6 and deficient in n-3 essential fatty acids is a major risk factor for diabetes and atherosclerosis [60].…”

Section: The Acute-phase Response and Diabetic Complicationsmentioning

confidence: 99%

Is Type II diabetes mellitus a disease of the innate immune system?

1998

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The cause of the common type of Type II (non-insulin-dependent) diabetes mellitus, which affects at least 100 million people throughout the world, is not known. One of the foremost challenges we face is to account mechanistically for not only the defining hyperglycaemia but also for the myriad of other biochemical and physiological abnormalities which are characteristic of this disease. For example, it is now clear that Type II diabetes and lesser degrees of glucose intolerance commonly occur together with a collection of clinical and biochemical features which have been called metabolic syndrome X [1, 2].These features include central obesity, hypertension, accelerated atherosclerosis, hypertriglyceridaemia and low serum concentrations of high-density lipoprotein (HDL) cholesterol. Though insulin resistance seems to be a central abnormality, the origin of the impaired insulin action and how it explains the many other abnormalities of Type II diabetes is not known.In recent years, we have been gathering evidence that in Type II diabetes there is a cytokine-associated acute-phase reaction, part of the innate immune response. As an alternative direction for research into the aetiology of Type II diabetes, we propose that it may be helpful to consider whether the mechanisms involved in the acute-phase response can be major contributors to the pathophysiology of many of the features of Type II diabetes and syndrome X, including glucose intolerance, insulin resistance, impair- Diabetologia (1998) Summary Type II (non-insulin-dependent) diabetes mellitus is associated with increased blood concentrations of markers of the acute-phase response, including sialic acid, a-1 acid glycoprotein, serum amyloid A, C-reactive protein and cortisol, and the main cytokine mediator of the response, interleukin-6. The dyslipidaemia common in Type II diabetes (hypertriglyceridaemia and low serum levels of HDL cholesterol) is also a feature of natural and experimental acutephase reactions. We review evidence that a long-term cytokine-mediated acute-phase reaction occurs in Type II diabetes and is part of a wide-ranging innate immune response. Through the action of cytokines on the brain, liver, endothelium, adipose tissue and elsewhere, this process could be a major contributor to the biochemical and clinical features of metabolic syndrome X (glucose intolerance, dyslipidaemia, insulin resistance, hypertension, central obesity, accelerated atherosclerosis) but also provides a mechanism for many other abnormalities seen in Type II diabetes, including those in blood clotting, the reproductive system, metal ion metabolism, psychological behaviour and capillary permeability. In the short-term, the innate immune system restores homeostasis after environmental threats; we suggest that in Type II diabetes and impaired glucose tolerance long-term lifestyle and environmental stimulants, probably in those with an innately hypersensitive acute-phase response, produce disease instead of repair. [Diabetologia (1998

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“…In addition to activating the immune system, a number of these molecules bring about metabolic changes in the subject which lead to the provision of nutrients for the activated immune system. The cytokines involved in this process are IL-1 and -6 and TNF-a and -p (Grimble, 1990). …”

mentioning

confidence: 99%

Dietary manipulation of the inflammatory response

Grimble

1992

Proc. Nutr. Soc.

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Nutrition and Cytokine Action

Cited by 97 publications

References 104 publications

Chronic Subclinical Inflammation as Part of the Insulin Resistance Syndrome

Chronic Subclinical Inflammation as Part of the Insulin Resistance Syndrome

Is Type II diabetes mellitus a disease of the innate immune system?

Dietary manipulation of the inflammatory response

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