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  • 1
    Online Resource
    Online Resource
    Cambridge University Press (CUP) ; 2013
    In:  Public Health Nutrition Vol. 16, No. 1 ( 2013-01), p. 27-35
    In: Public Health Nutrition, Cambridge University Press (CUP), Vol. 16, No. 1 ( 2013-01), p. 27-35
    Abstract: Despite extensive research into the biological mechanisms behind obesity-related inflammation, knowledge of environmental and genetic factors triggering such mechanisms is limited. In the present narrative review we present potential determinants of adipose tissue inflammation and suggest ways ahead for future research in the field. Design We searched the literature for potential determinants of obesity with inflammation through MEDLINE by applying the MeSH headings ‘obesity’ and ‘inflammation’ in combination with specific terms for a series of environmental and genetic factors. Results Numerous articles reported on the association between environmental or genetic factors and respectively obesity and inflammation, whereas only a few studies assessed obesity and inflammation as a combined outcome. Among suggested determinants for obesity with inflammation were Adenovirus-36, the gut microbiota, trans -fatty acids, and the four genes FTO , MC4R , TNF-α and LEPR . Conclusions We present a limited number of factors potentially contributing to the development of obesity with inflammation, while concluding that overall the area is indeed sparsely investigated. We present ideas for future studies that can identify relevant aetiological factors. This identification is essential for targeted prevention of obesity with inflammation and the clinical consequences thereof.
    Type of Medium: Online Resource
    ISSN: 1368-9800 , 1475-2727
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2013
    detail.hit.zdb_id: 2016337-X
    SSG: 21
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  • 2
    In: British Journal of Nutrition, Cambridge University Press (CUP), Vol. 106, No. 8 ( 2011-10-28), p. 1245-1252
    Abstract: Intake of trans- fatty acids (TFA), especially industrially produced TFA (I-TFA), has been associated with the risk of CHD through influence on serum lipid levels. Other causal pathways remain less investigated. In the present cross-sectional study of middle-aged men representing a broad range of BMI, the association between intake of TFA, I-TFA and ruminant TFA (R-TFA) and obesity-associated risk markers of CHD was assessed. The study comprised 393 Danish men (median age 49 years) with a median BMI of 28·4 kg/m 2 . Intake of TFA was estimated based on 7 d dietary records, whereas outcomes of interest (waist circumference, sagittal abdominal diameter, percentage of truncal fat, C-reactive protein, IL-6, blood lipids, blood pressure, HbA1c and insulin sensitivity index) were obtained through clinical examination. The associations were assessed by linear regression analysis. The median intake of total TFA among the 393 men was 1·3 g/d, covering a daily I-TFA intake of 0·4 g (10–90th percentile 0·0–1·0) and R-TFA intake of 0·9 g (10–90th percentile 0·4–1·8). Intake of these amounts of TFA showed no significant associations with abdominal fatness, inflammatory markers, blood lipids, blood pressure and insulin homeostasis. Among middle-aged men with a generally low intake of TFA, neither I-TFA nor R-TFA was significantly related to obesity-associated risk markers of CHD. The decreased average intake of I-TFA in Denmark since 1995 is suggested to effectively prevent occurrence of the adverse metabolic changes and health consequences, which have formerly been observed in relation to, especially, I-TFA intake.
    Type of Medium: Online Resource
    ISSN: 0007-1145 , 1475-2662
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2011
    detail.hit.zdb_id: 2016047-1
    SSG: 12
    SSG: 21
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