CLOCK genetic variation and metabolic syndrome risk: modulation by monounsaturated fatty acids

Garaulet, Marta; Lee, Yu Chi; Shen, Jian; Parnell, Laurence D.; Arnett, Donna K.; Tsai, Michael Y.; Lai, Chao‐Qiang; Ordovas, José M.

doi:10.3945/ajcn.2009.27536

Cited by 147 publications

(153 citation statements)

References 56 publications

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“…Additionally, the importance of individual differences in phase and amplitude of lipid rhythms has yet to be explored. Several epidemiologic studies suggest that genetic variation in clock genes modulates risk for obesity and type 2 diabetes (116)(117)(118)(119) , but the underlying mechanisms are poorly understood. Therefore, future studies should examine the interaction of genetic and environmental factors on diurnal regulation of lipids and postprandial responses.…”

Section: Limitations and Future Directionsmentioning

confidence: 99%

Circadian regulation of lipid metabolism

Gooley

2016

Proc. Nutr. Soc.

134

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The circadian system temporally coordinates daily rhythms in feeding behaviour and energy metabolism. The objective of the present paper is to review the mechanisms that underlie circadian regulation of lipid metabolic pathways. Circadian rhythms in behaviour and physiology are generated by master clock neurons in the suprachiasmatic nucleus (SCN). The SCN and its efferent targets in the hypothalamus integrate light and feeding signals to entrain behavioural rhythms as well as clock cells located in peripheral tissues, including the liver, adipose tissue and muscle. Circadian rhythms in gene expression are regulated at the cellular level by a molecular clock comprising a core set of clock genes/proteins. In peripheral tissues, hundreds of genes involved in lipid biosynthesis and fatty acid oxidation are rhythmically activated and repressed by clock proteins, hence providing a direct mechanism for circadian regulation of lipids. Disruption of clock gene function results in abnormal metabolic phenotypes and impaired lipid absorption, demonstrating that the circadian system is essential for normal energy metabolism. The composition and timing of meals influence diurnal regulation of metabolic pathways, with food intake during the usual rest phase associated with dysregulation of lipid metabolism. Recent studies using metabolomics and lipidomics platforms have shown that hundreds of lipid species are circadian-regulated in human plasma, including but not limited to fatty acids, TAG, glycerophospholipids, sterol lipids and sphingolipids. In future work, these lipid profiling approaches can be used to understand better the interaction between diet, mealtimes and circadian rhythms on lipid metabolism and risk for obesity and metabolic diseases.

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Section: Limitations and Future Directionsmentioning

confidence: 99%

Circadian regulation of lipid metabolism

Gooley

2016

Proc. Nutr. Soc.

134

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“…For example, CLOCK SNP (rs3749474, rs4580704 and rs1801260 (3111T > C)) were associated with BMI, energy intake and different variables related to obesity (14) . In fact, our results showed that carriers of the minor alleles consumed more energy (15) (1046 kJ (250 kcal)/d, ate more fat (5-10 g), and were more obese (3 kg body weight) for rs3749474, rs1801260 (3111T > C)).…”

Section: Failures In the Central Clock: Mutations In Experimental Animentioning

confidence: 99%

“…In fact, over the last few years it has been demonstrated that different SNP in our circadian machinery interact with dietary intake and several behaviours for obesity and for other metabolic risk (MetS)-related variables (8,14,31) . In this sense, in 2009 we revealed several interactions between CLOCK variants and dietary intakes for different Table 1.…”

Section: Nutrigenetics Says: Our Genome May Interact With Our Behavioursmentioning

confidence: 99%

“…In minor alleles carriers: -Decrease energy intake -Decrease total fat intake (14) CLOCK rs1801260 (3111T > C)…”

Section: Evidences In Nutrigeneticmentioning

confidence: 99%

“…2. SFA for waist circumference (among C allele carriers when the SFA energy intake was more than 11·8 % had higher waist circumference) Among C allele carriers the 'emotional eaters': -Develop a stronger follow up plan during dietary therapy -Try to have SFA energy intake lower than 11·8 % (8,14) CLOCK rs4580704…”

Section: Evidences In Nutrigeneticmentioning

confidence: 99%

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Circadian rhythms, food timing and obesity

2016

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It is known that our physiology changes throughout the day and that several physiological hormones display circadian rhythmicity. The alteration of this normal pattern is called chronodisruption (CD). In recent years, it has been demonstrated that CD is related to obesity. Although several factors may be causing CD, one important aspect to consider is the failure in our internal clock. Indeed, studies performed in mutant animals have demonstrated that mutations in clock genes are related to obesity. In human subjects, mutations are rare (<1 % of the population). Nevertheless, it is rather common to have genetic variations in one SNP, which underlie differences in our vulnerability to disease. Several SNP in clock genes are related to obesity and weight loss. Taking into account that genetics is behind CD, as has already been demonstrated in twins’ models, the question is: Are we predestinated? We will see along these lines that nutrigenetics and epigenetics answer: ‘No, we are not predestinated’. Through nutrigenetics we know that our behaviours may interact with our genes and may decrease the deleterious effect of one specific risk variant. From epigenetics the message is even more positive: it is demonstrated that by changing our behaviours we can change our genome. Herein, we propose modifying ‘what, how, and when we eat’ as an effective tool to decrease our genetic risk, and as a consequence to diminish CD and decrease obesity. This is a novel and very promising area in obesity prevention and treatment.

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Plasma phospholipids n‐3 polyunsaturated fatty acid is associated with metabolic syndrome

Huang

Subhachai

Cai

et al. 2010

Molecular Nutrition Food Res

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The relationship between n-3 PUFA and metabolic syndrome (MS) is not clear. The aim of this study was to examine relationships between plasma phospholipids (PL) n-3 PUFA and MS in Chinese subjects. Nine hundred and twenty-nine subjects were recruited in Hangzhou, China. Two hundred and ten (183 males, 27 females) with MS and 719 (545 males, 174 females) healthy subjects were identified in this cross-sectional study. The prevalence of MS in females (24.56%) was significantly higher than that in males (10.04%) in this population. Total PUFA (p<0.001), n-3 PUFA (p<0.001), and n-3:n-6 (p<0.001) were significantly lower in MS subjects compared to healthy subjects. Plasma phospholipid (PL), n-3 PUFA was significantly inversely associated with MS (p = 0.013). In addition, subjects with high levels of PL total fatty acids (FA) had a more than threefold higher likelihood of MS (OR = 3.44, 95% CI = 1.60-7.39) than the subjects with low levels of PL total FA. Our results suggest that plasma PL n-3 PUFA was significantly inversely associated with MS, while high total FA were positively associated with MS in Chinese.

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CLOCK genetic variation and metabolic syndrome risk: modulation by monounsaturated fatty acids

Abstract: CLOCK polymorphisms interact with FAs to modulate MetS traits. The dietary source and membrane content of MUFAs are implicated in the relations between alterations in the circadian system and MetS.

Cited by 147 publications

References 56 publications

Circadian regulation of lipid metabolism

Circadian regulation of lipid metabolism

Circadian rhythms, food timing and obesity

Plasma phospholipids n‐3 polyunsaturated fatty acid is associated with metabolic syndrome

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