Genetics and epigenetics in obesity

Rohde, Kerstin; Keller, Maria; Poulsen, Lars la Cour; Blüher, Matthias; Kovacs, Peter; Böttcher, Yvonne

doi:10.1016/j.metabol.2018.10.007

Cited by 272 publications

(219 citation statements)

References 152 publications

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“…1 Many different factors contribute to the metabolic consequences of obesity, including complex interactions between genetics, environment and lifestyle aspects, in which environmental factors may play critical roles as shown in large populations. 2 Recent research indicates that the gut microbiota can be considered an environmental factor and/or an integrator of environmental triggers that contribute to fat mass and obesity development. 3 4 Several human studies have now investigated the relationship between the human gut microbiota and obesity phenotypes [5][6][7] and a meta-analysis has shown significant associations between decreased alpha diversity, obesity and obesity severity.…”

Section: Introductionmentioning

confidence: 99%

Gut microbiota of obese subjects with Prader-Willi syndrome is linked to metabolic health

Olsson

Poitou

Tremaroli

et al. 2019

Gut

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ObjectiveThe gut microbiota has been implicated in the aetiology of obesity and associated comorbidities. Patients with Prader-Willi syndrome (PWS) are obese but partly protected against insulin resistance. We hypothesised that the gut microbiota of PWS patients differs from that of non-genetically obese controls and correlate to metabolic health. Therefore, here we used PWS as a model to study the role of gut microbiota in the prevention of metabolic complications linked to obesity.DesignWe conducted a case-control study with 17 adult PWS patients and 17 obese subjects matched for body fat mass index, gender and age. The subjects were metabolically characterised and faecal microbiota was profiled by 16S ribosomal RNA gene sequencing. The patients’ parents were used as a non-obese control group. Stool samples from two PWS patients and two obese controls were used for faecal microbiota transplantations in germ-free mice to examine the impact of the microbiota on glucose metabolism.ResultsThe composition of the faecal microbiota in patients with PWS differed from that of obese controls, and was characterised by higher phylogenetic diversity and increased abundance of several taxa such as Akkermansia, Desulfovibrio and Archaea, and decreased abundance of Dorea. Microbial taxa prevalent in the PWS microbiota were associated with markers of insulin sensitivity. Improved insulin resistance of PWS was partly transmitted by faecal microbiota transplantations into germ-free mice.ConclusionThe gut microbiota of PWS patients is similar to that of their non-obese parents and might play a role for the protection of PWS patients from metabolic complications.

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Section: Introductionmentioning

confidence: 99%

Gut microbiota of obese subjects with Prader-Willi syndrome is linked to metabolic health

Olsson

Poitou

Tremaroli

et al. 2019

Gut

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“…Уровень лептина сыворотки крови достоверно коррелирует с количеством жировой ткани в организме. Объем жировой ткани и пол человека -основные факторы, определяющие экспрессию гена лептина [18]. У женщин уровень лептина сыворотки крови выше, чем у мужчин [19], что может быть связано с особенностями распределения жировой ткани, а также стимулирующим эффектом эстрогенов, прогестерона и подавляющим влиянием андрогенов [20].…”

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Subcutaneous and Epicardial Adipose Tissue Leptin Gene Expression in Coronary Artery Disease Patient

Полякова

Колодина

Miroshnikova

et al. 2019

Transl. med. (Print)

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Objective. To assess the expression of the leptin gene (LEP) in the epicardial (EAT) and subcutaneous (SAT) adipose tissue in coronary artery disease (CAD) patients.Methods. 107 people were examined: 87 with CAD (57 men, 30 women), 20 without CAD (10 men, 10 women). Biopsy of EAT, SAT, coronary angiography, heart computed tomography, blood leptin levels were estimate, mRNA expression of the LEP gene evaluated by PCR.Results. In CAD patients with multivessel coronary artery lesion, the level of blood leptin is the highest. The expression of the LEP gene in EAT is higher in men than in women, in men with CAD higher than in non-coronary artery disease patients, and with a multivascular coronary lesion higher than in a 1–2 vascular lesion. Expression of the LEP gene in EAT in women with CAD is higher than with no CAD, and does not depend on the severity of coronary atherosclerosis. In SAT, LEP gene expression in men with CAD is higher than without CAD; women with CAD are lower than without CAD. Expression of the LEP gene in SAT is higher in men with a multivascular lesion than in 1–2 vascular lesion, and lower in women with a multivascular damage.Conclusions. The expression of the leptin gene in women is higher in SAT, and in men in EAT. Expression of the leptin gene in EAT with CAD is higher than without CAD. The expression of the leptin gene in SAT in men with CAD, especially with multivessel lesions, is higher than without coronary artery disease.

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“…These effects are observed during both the prenatal and postnatal period, reflecting effects that occur through intrauterine mechanisms and lactation. Our findings likely reflect greater complexity of appetite regulation in humans, involving environmental, psychosocial, and genetic drivers that are an active area of research . Additionally, we were not able to examine associations between postnatal factors (eg, lactation) and eating behaviours.…”

Section: Discussionmentioning

confidence: 89%

Prenatal predictors of objectively measured appetite regulation in low‐income toddlers and preschool‐age children

et al. 2019

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Summary Background Prenatal nutrition impacts offspring appetite regulation in animal models. However, evidence from humans is scarce. Objective To determine associations between indicators of prenatal nutrition and appetite regulation among young children. Methods Participants included 454 low‐income mother/child dyads (mean child age = 45.2 months [SD = 9.7]). Children's appetite regulation was ascertained with the maternal‐reported Child Eating Behavior Questionnaire and objectively assessed using the Eating in the Absence of Hunger protocol. Using hierarchical linear regression, we modelled child appetite regulation measures as a function of prenatal nutrition indicators (child birthweight z scores [BWz, BWz2]; maternal pre‐pregnancy body mass index [BMI], gestational weight gain [GWG]), adjusted for sociodemographic characteristics. Results Among girls, higher and lower birthweight were associated with greater energy consumed in the absence of hunger, primarily sweet foods, coeff (95% CI): BWz 0.17 (0.05, 0.28), BWz2 0.15 (0.04, 0.26), but not food responsiveness or food enjoyment. Higher birthweight was also associated with greater satiety responsiveness among girls. Among boys, birthweight was unrelated to measures of appetite regulation. Associations between maternal BMI and GWG and child appetite regulation were inconsistent. Conclusions Among low‐income girls, but not boys, indicators of adverse prenatal conditions were associated with poor objectively measured appetite regulation during early childhood.

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Genetics and epigenetics in obesity

Cited by 272 publications

References 152 publications

Gut microbiota of obese subjects with Prader-Willi syndrome is linked to metabolic health

Gut microbiota of obese subjects with Prader-Willi syndrome is linked to metabolic health

Subcutaneous and Epicardial Adipose Tissue Leptin Gene Expression in Coronary Artery Disease Patient

Prenatal predictors of objectively measured appetite regulation in low‐income toddlers and preschool‐age children

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