DNA Microarray Analysis of Genes Differentially Expressed in Diet‐Induced (Cafeteria) Obese Rats

López, Icíar P.; Martí, Amelia; Milagro, Fermı́n I.; Zulet, María de Los Ángeles; Moreno-Aliaga, María J.; Martínéz, J. Alfredo; Miguel, Carlos de

doi:10.1038/oby.2003.30

Cited by 144 publications

(106 citation statements)

References 21 publications

(25 reference statements)

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“…The key factors are the PPARg, particularly the adipose-specific isoform PPARg2 (37,38) . In a metaanalysis examining the Pro12Ala polymorphism in 19 136 subjects a positive association with BMI has been found (3) .…”

Section: Genes Encoding Factors Implicated In Adipogenesismentioning

confidence: 99%

Interaction between genes and lifestyle factors on obesity

2008

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Obesity originates from a failure of the body-weight control systems, which may be affected by changing environmental influences. Basically, the obesity risk depends on two important mutually-interacting factors: (1) genetic variants (single-nucleotide polymorphisms, haplotypes); (2) exposure to environmental risks (diet, physical activity etc.). Common singlenucleotide polymorphisms at candidate genes for obesity may act as effect modifiers for environmental factors. More than 127 candidate genes for obesity have been reported and there is evidence to support the role of twenty-two genes in at least five different populations. Geneenvironment interactions imply that the synergy between genotype and environment deviates from either the additive or multiplicative effect (the underlying model needs to be specified to appraise the nature of the interaction). Unravelling the details of these interactions is a complex task. Emphasis should be placed on the accuracy of the assessment methods for both genotype and lifestyle factors. Appropriate study design (sample size) is crucial in avoiding false positives and ensuring that studies have enough power to detect significant interactions, the ideal design being a nested case-control study within a cohort. A growing number of studies are examining the influence of gene-environmental interactions on obesity in either epidemiological observational or intervention studies. Positive evidence has been obtained for genes involved in adiposity, lipid metabolism or energy regulation such as PPARg2 (Pro12Ala), b-adrenoceptor 2 (Gln27Glu) or uncoupling proteins 1, 2 and 3. Variants on other genes relating to appetite regulation such as melanocortin and leptin receptors have also been investigated. Examples of some recently-identified interactions are discussed.Obesity risk: Mutations: Physical activity: Diet: Gene-environment interaction Genetics of obesityNowadays, the availability of genomics technology represents a major advance in the study of the genetics of obesity (1,2) . Human genetic differences appear at the level of single-nucleotide polymorphisms, copy-number polymorphisms and the specific combinations of alleles (haplotypes) (3,4) . The configuration of multiple genes can range from polygenic (i.e. many genes with a relatively small contribution) to oligogenic (i.e. few genes with large measurable effects often expressed on a residual polygenic background). Indeed, it is this oligogenic architecture that has justified the current efforts to map genes for complex phenotypes. In the present paper the influence of a number of single-nucleotide polymorphisms in genes encoding factors regulating food and energy intake and factors implicated in energy expenditure and adiposity will be summarised. Genes encoding factors regulating food and energy intakeIt is generally accepted that hypothalamic and brain stem centres are involved in the regulation of food intake and energy balance but only in the last decade has information on the relevant regulatory factors and their genes ...

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Section: Genes Encoding Factors Implicated In Adipogenesismentioning

confidence: 99%

Interaction between genes and lifestyle factors on obesity

2008

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“…Male Wistar rats (250-300 g), purchased from the Applied Pharmacobiology Center (CIFA, University of Navarra, Spain), were housed under controlled conditions of temperature (22 ± 2°C), relative humidity (55 ± 10%) and light cycle (8 a laboratory pelleted diet (Harlan Iberica, Barcelona, Spain), whereas the second group (n = 28) was fed a fat-rich cafeteria diet [10]. Rats were sacrificed by decapitation, after overnight fasting, in four moments during the experimental period: 4, 12, 35 and 72 days.…”

Section: Animals Diets and Experimental Designmentioning

confidence: 99%

Time‐dependent regulation of muscle caveolin activation and insulin signalling in response to high‐fat diet

et al. 2009

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a b s t r a c tWe studied the effect of high-fat diet on the expression and activation of the three caveolins in rat skeletal muscle and their association with the insulin signalling cascade. Initial response was characterized by increased signalling through Cav-1 and Cav-3 phosphorylation, suggesting that both participate in an initial acute response to the calorie surplus. Afterwards, Cav-1 signalling was slightly reduced, whereas Cav-3 remained active. Late chronic phase signalling through both proteins was impaired inducing a prediabetic state. Summarizing, caveolins seem to mediate a timedependent regulation of insulin cascade in response to high-fat diet in muscle.

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“…On the other hand, fatty acids play a central role in the induction of mesenchymal stromal cells (MSC) to adipocyte differentiation, as well as in adipose tissue hypertrophy, because they have the ability to activate the peroxisome proliferator-activated receptor gamma (PPARc), which is a transcription factor inducing adipogenesis (Lopez et al 2003;Shillabeer and Lau 1994). We have previously shown that AA promotes a greater degree of adipocyte differentiation of MSC than DHA or EPA (Casado-Diaz et al 2013).…”

Section: Introductionmentioning

confidence: 99%

Effects of arachidonic acid on the concentration of hydroxyeicosatetraenoic acids in culture media of mesenchymal stromal cells differentiating into adipocytes or osteoblasts

et al. 2013

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Metabolites derived from the polyunsaturated fatty acids (PUFA) may modulate the mesenchymal stromal cell (MSC) differentiation. Such cells can differentiate into different cellular types, including adipocytes and osteoblasts. Aging favors the bone marrow MSC differentiation toward the former, causing a loss of bone density associated with pathologies like osteoporosis. The omega-6 arachidonic acid (AA) favors MSC adipogenesis to a greater extent than omega-3 eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA). In this work, we study the joint action of both PUFA. Thus, not induced and induced to adipocyte or osteoblast MSC were treated with 20 lM of each PUFA (either AA, AA ? DHA or AA ? EPA). The expression of osteogenic and adipogenic molecular markers, the alox15b lipoxygenase gene expression and the 5-, 8-, 11-, 12-and 15-hydroxyeicosatetraenoic acids (HETE) derived from the AA metabolism in the culture media were determined. The results show that the adipogenesis induction of AA is not suppressed by the joint presence of EPA and DHA. In fact, both increased the adipogenic effect of AA on MSC differentiated into osteoblasts. The different HETE concentrations increased in cultures supplemented with AA, albeit such concentrations were lower in the cultures induced to differentiate, mainly at day 21 after the induction. Furthermore, the reduction in the HETE concentration was correlated with a higher expression of the alox15b gene. These results highlight the PUFA metabolism differences between uninduced and induced MSC to differentiate into adipocytes and osteoblasts, besides the relevant role of the lipoxygenase gene expression in adipogenesis induction.

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DNA Microarray Analysis of Genes Differentially Expressed in Diet‐Induced (Cafeteria) Obese Rats

Cited by 144 publications

References 21 publications

Interaction between genes and lifestyle factors on obesity

Interaction between genes and lifestyle factors on obesity

Time‐dependent regulation of muscle caveolin activation and insulin signalling in response to high‐fat diet

Effects of arachidonic acid on the concentration of hydroxyeicosatetraenoic acids in culture media of mesenchymal stromal cells differentiating into adipocytes or osteoblasts

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