| 1. |
- Hanson, Lars Åke, 1934, et al.
(author)
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Growth and nutrition: the first six months
- 2008
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In: Nestlé Nutrition workshop series. Paediatric programme. - Basel : KARGER. - 1661-6677. ; 61, s. 123-34
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Journal article (other academic/artistic)abstract
- Today the WHO Growth Chart Standards, based on the growth of breastfed infants, are used. These growth curves solve the problem of the deviating observations for breastfed compared to non-breastfed infants using previous growth charts. Presently it is not clear how the mother's diet, especially the fat intake, influences the growth of the offspring. Animal experiments indicate that a low intake of n-3 polyunsaturated fatty acids via the milk may have short- and long-term negative consequences. There is limited information in man. It has been suggested that the mammary glands may have phylogenetically originated from glands providing innate immunity, later developing capacities for providing nutrition. This would agree with the fact that human milk contains so many major components which do not primarily function as nutrients, but seem to protect nutrition and growth. Lactoferrin, oligosaccharides, glycoproteins, secretory IgA antibodies, alpha-lactalbumin and the antisecretory factor have such functions.
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| 2. |
- Hanson, Lars Åke, 1934, et al.
(author)
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Immune function
- 2009
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In: Advances in experimental medicine and biology. - 0065-2598 .- 2214-8019. ; 639, s. 97-111
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Journal article (other academic/artistic)
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| 3. |
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| 4. |
- Håversen, Liliana, 1963, et al.
(author)
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Induction of proinflammatory cytokines by long-chain saturated fatty acids in human macrophages.
- 2009
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In: Atherosclerosis. - : Elsevier BV. - 1879-1484 .- 0021-9150. ; 202:2, s. 382-93
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Journal article (peer-reviewed)abstract
- Increased circulating free fatty acids in subjects with type 2 diabetes may contribute to activation of macrophages, and thus the development of atherosclerosis. In this study, we investigated the effect of the saturated fatty acids (SFA) palmitate, stearate, myristate and laurate, and the unsaturated fatty acid linoleate, on the production of proinflammatory cytokines in phorbol ester-differentiated THP-1 cells, a model of human macrophages. Palmitate induced secretion and mRNA expression of TNF-alpha, IL-8 and IL-1 beta, and enhanced lipopolysaccharide (LPS)-induced IL-1 beta secretion. Proinflammatory cytokine secretion was also induced by stearate, but not by the shorter chain SFA, myristate and laurate, or linoleate. Triacsin C abolished the palmitate-induced cytokine secretion, suggesting that palmitate activation to palmitoyl-CoA is required for its effect. Palmitate-induced cytokine secretion was decreased by knockdown of serine palmitoyltransferase and mimicked by C(2)-ceramide, indicating that ceramide is involved in palmitate-induced cytokine secretion. Palmitate phosphorylated p38 and JNK kinases, and blocking of these kinases with specific inhibitors diminished the palmitate-induced cytokine secretion. Palmitate also activated the AP-1 (c-Jun) transcription factor. Knockdown of MyD88 reduced the palmitate-induced IL-8, but not TNF-alpha or IL-1 beta secretion. In conclusion, our data suggest that the long-chain SFA induce proinflammatory cytokines in human macrophages via pathways involving de novo ceramide synthesis. This might contribute to the activation of macrophages in atherosclerotic plaques, especially in type 2 diabetes.
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| 5. |
- Wiklund, Olov, 1943, et al.
(author)
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How can we prevent cardiovascular disease in diabetes
- 2007
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In: Journal of Internal Medicine. - : Wiley. - 0954-6820 .- 1365-2796. ; 262:2, s. 199-207
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Journal article (peer-reviewed)abstract
- Evidence based goals for the treatment and prevention of atherosclerosis in diabetes are given in international and national guidelines. The importance of optimal control of lipids and blood pressure has been shown in several studies. With available drugs and behavioural modifications the treatment goals can be reached in most cases. However, only a few patients with diabetes are treated optimally today. A major possibility to reduce cardiovascular disease in diabetes is to treat patients according to guidelines. New treatment targets may include specific treatment of the dyslipidaemia, manifested in high levels of small dense LDL and low HDL, active anti-inflammatory treatments, specific reduction of inflammatory activity in adipose tissue, reduced volume of adipose tissue, antioxidants and reduction of advanced glycosylation endproducts production. Possible strategies for these treatments are available, and should be evaluated in clinical trials.
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