| 1. |
- Jonasson, Lena, et al.
(författare)
-
Advice to follow a low-carbohydrate diet has a favourable impact on low-grade inflammation in type 2 diabetes compared with advice to follow a low-fat diet
- 2014
-
Ingår i: Annals of Medicine. - : Informa Healthcare. - 0785-3890 .- 1365-2060. ; 46:3, s. 182-187
-
Tidskriftsartikel (refereegranskat)abstract
- BACKGROUND: Inflammation may play an important role in type 2 diabetes. It has been proposed that dietary strategies can modulate inflammatory activity.METHODS: We investigated the effects of diet on inflammation in type 2 diabetes by comparing a traditional low-fat diet (LFD) with a low-carbohydrate diet (LCD). Patients with type 2 diabetes were randomized to follow either LFD aiming for 55-60 energy per cent (E%) from carbohydrates (n = 30) or LCD aiming for 20 E% from carbohydrates (n = 29). Plasma was collected at baseline and after 6 months. C-reactive protein (CRP), interleukin-1 receptor antagonist (IL-1Ra), IL-6, tumour necrosis factor receptor (TNFR) 1 and TNFR2 were determined.RESULTS: Both LFD and LCD led to similar reductions in body weight, while beneficial effects on glycaemic control were observed in the LCD group only. After 6 months, the levels of IL-1Ra and IL-6 were significantly lower in the LCD group than in the LFD group, 978 (664-1385) versus 1216 (974-1822) pg/mL and 2.15 (1.65-4.27) versus 3.39 (2.25-4.79) pg/mL, both P < 0.05.CONCLUSIONS: To conclude, advice to follow LCD or LFD had similar effects on weight reduction while effects on inflammation differed. Only LCD was found significantly to improve the subclinical inflammatory state in type 2 diabetes.
|
|
| 2. |
- Jönsson, Simon, et al.
(författare)
-
Glucocorticoid sensitivity and inflammatory status of peripheral blood mononuclear cells in patients with coronary artery disease
- 2018
-
Ingår i: Annals of Medicine. - : TAYLOR & FRANCIS LTD. - 0785-3890 .- 1365-2060. ; 50:3, s. 260-268
-
Tidskriftsartikel (refereegranskat)abstract
- Objective: Mechanisms behind sustained inflammation in patients with coronary artery disease (CAD) are not clarified but hypothalamus-pituitary-adrenal (HPA) axis dysfunction may have a role. Here, we investigated whether inflammatory status of peripheral blood mononuclear cells (PBMCs) was associated with altered glucocorticoid sensitivity in CAD patients. Methods: In 55 CAD patients and 30 controls, mRNA levels of GR-alpha, GR-beta, NF-kappa B, I kappa B alpha, MMP-9 and TIMP-1 were measured in PBMCs. Suppressive effects of dexamethasone on GR-alpha, GR-beta, NF-kappa B, I kappa B alpha, MMP-9 and TIMP-1 mRNA levels were assessed in PBMCs ex vivo. Salivary cortisol was repeatedly measured over 3 days. Results: GR-alpha mRNA levels were higher in CAD patients than in controls, 0.50 (0.38-0.59) versus 0.26 (0.18-0.37), pamp;lt;.001, while GR-beta mRNA levels were equally low in both groups. GR-alpha mRNA expression was associated with inflammatory gene expression and, also, with flatter diurnal cortisol rhythm. In both patients and controls, dexamethasone suppressed gene expression of NF-B, IB, MMP-9 and TIMP-1 (p amp;lt; .001). Dexamethasone also reduced GR-alpha mRNA levels (p amp;lt; .001), while LPS increased it (p amp;lt; .001). Conclusions: PBMCs from CAD patients displayed an inflammatory gene expression profile. This was not explained by reduced glucocorticoid sensitivity. Instead, inflammation was associated with increased expression of GR-alpha mRNA, suggesting a hypocortisolemic state.
|
|
| 3. |
- Nijm, Johnny, et al.
(författare)
-
Inflammation and cortisol response in coronary artery disease
- 2009
-
Ingår i: ANNALS OF MEDICINE. - : Informa UK Limited. - 0785-3890 .- 1365-2060. ; 41:3, s. 224-233
-
Tidskriftsartikel (refereegranskat)abstract
- Atherosclerosis is characterized by chronic inflammation involving autoimmune components. The degree of inflammatory activity, as detectable both within the atherosclerotic plaque and in the circulation, is associated with plaque destabilization and atherothrombotic complications. Endogenous glucocorticoids are modulators of innate and acquired immune responses, and as such play a key role in the reciprocal interaction between neuroendocrine and immune systems. Abnormalities in hypothalamic-pituitary-adrenal axis (HPA) function have been described in several chronic inflammatory disorders, and evidence has emerged lately that HPA dysfunction may be implicated also in the pathogenesis of coronary artery disease. This review is an outline of knowledge gained so far by previous studies of glucocorticoids in coronary atherosclerosis and myocardial infarction. The results consistently point towards a dysregulated cortisol secretion that may involve a failure to contain inflammatory activity. A dysfunctional HPA axis and its possible implications for coronary artery disease progress, including the hypothetical link between stress and inflammation, are discussed.
|
|
