Associations of ADIPOQ and LEP Gene Variants with Energy Intake: A Systematic Review

Kroll, Caroline; Mastroeni, Silmara S. B. S.; Veugelers, Paul J.; Mastroeni, Marco Fábio

doi:10.3390/nu11040750

Cited by 14 publications

(11 citation statements)

References 71 publications

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“…4,5,20 The rs17300539 adiponectin gene, an adipokine abundantly produced by adipose tissue, was associated with a decrease in the serum expression of adiponectin in adults. 7,22 In our study, this decrease was also observed in obese children and adolescents. Adiponectin participates in energy homeostasis and acts on adipose tissue, and reduction in adiponectin concentrations promotes sluggish lipid and carbohydrate metabolism, thereby stimulating the consumption of food for energy supply.…”

Section: Discussionsupporting

confidence: 79%

“…necessary to investigate this relationship in children and adolescents with these polymorphisms and measure the consequences on body weight and health. [5][6][7] Therefore, the objective of this study was to compare anthropometric, biochemical, and hormonal parameters and the presence of genetic polymorphisms of leptin, adiponectin, and TNF-α among eutrophic and obese children and adolescents.…”

Section: Discussionmentioning

confidence: 99%

“…Serum leptin production and concentration are proportional to adipose tissue mass. [4][5][6][7] In contrast, the adiponectin gene produces a protein exclusively transcribed in adipose tissue. It reduces TNF-α expression, decreases macrophage chemotaxis, inhibits monocyte adhesion and macrophage transformation into foam cells, increases nitric oxide production, and stimulates angiogenesis.…”

Section: Introductionmentioning

confidence: 99%

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Genetic polymorphisms and plasma concentrations of leptin (rs7799039) and adiponectin (rs17300539) are associated with obesity in children and adolescents

Menezes

Alves-Junior

Costa

et al. 2022

Rev. paul. pediatr.

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Objective: The aim of this study was to compare the anthropometric, biochemical, and hormonal characteristics and the presence of genetic polymorphisms of leptin, adiponectin, and tumor necrosis factor alpha (TNF-α) between eutrophic and obese children and adolescents. Methods: This is a case–control study involving 104 children and adolescents. All subjects were assessed for anthropometric characteristics and clinical, laboratory, and genetic polymorphism parameters. The sample was selected from the pediatric endocrinology outpatient clinic specialized in the treatment of obesity in children and adolescents according to the Centers for Disease Control and Prevention (CDC) classification, and controls were selected from the same location in the general pediatric outpatient clinic. Results: As a result, the parameters, such as black color, obese parents, hypertensive parents, and early weaning, were found to be associated with obesity. Increased levels of insulin, triglyceride, total cholesterol, LDL cholesterol, CRP-U, AST, ALT, GGT, free T4, IGF-1, and uric acid and low levels of HDL cholesterol are found to be associated with a higher chance of obesity. The presence of AG/AA polymorphisms in the leptin is associated with a 290% (OR 3.9) higher chance of obesity, and for adiponectin genes, the chances are 740% (OR 8.4) higher. In these obese children and adolescents with AG/AA haplotypes, serum leptin levels were increased and adiponectin levels were decreased in eutrophic individuals, whereas serum TNF-α levels did not change. Conclusions: The AG/AA polymorphisms in the leptin and adiponectin genes alter the serum levels of these adipokines and predispose them to obesity, and many anthropometric, biochemical, and hormonal markers are altered, demonstrating early consequences for the health of these obese children and adolescents.

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Section: Discussionsupporting

confidence: 79%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Genetic polymorphisms and plasma concentrations of leptin (rs7799039) and adiponectin (rs17300539) are associated with obesity in children and adolescents

Menezes

Alves-Junior

Costa

et al. 2022

Rev. paul. pediatr.

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“…Adiponectin regulates several metabolic processes, including glucose homoeostasis and fatty acid oxidation (1) . The decrease in serum adiponectin concentration mediated by genetic variation promotes a reduction in the phosphorylation of target proteins by AMP-activated protein kinase (AMPK), which is critical for lipid and carbohydrate metabolism (13,22,48,49) . Therefore, the involvement of the metabolism of many tissues may decrease energy consumption and stimulate food intake (48) .…”

Section: Discussionmentioning

confidence: 99%

Adiponectin and leptin gene variants and their effects on body weight trajectories in children from birth to 6 years of age: the PREDI Study

Kroll¹,

Farias²,

Kac³

et al. 2020

Br J Nutr

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Excess body weight confers a high risk to human health. Body weight variation between subjects can be partially explained by genetic differences. The aim of this study was to investigate the association of genetic variants in the ADIPOQ (rs2241766) and LEP (rs7799039) genes with body weight trajectories in children from birth to six years of age. This was a prospective cohort (PREDI Study). Socioeconomic, biological and anthropometric data were collected at four time points: at birth in the maternity unit; 1-2 years old, 4-5 years old, and 6 years old at the participant’s home. Genotyping was performed by PCR-RFLP. Poisson regression and linear mixed-effect regression models were used to address the association of ADIPOQ and LEP genotypes with BMI. Excessive body weight at pre-pregnancy (β=0.339, p=0.01) and excessive gestational weight gain (β=0.51, p<0.001) were associated with children’s BMI trajectory from birth to six years. The ADIPOQ-rs2241766 TG or GG genotype was associated with a higher risk of excess body weight in the first six years of life (both sexes: RR=1.25, 95%CI: 1.01-1.56; female: RR=1.67, 95%CI: 1.20-2.31). BMI increased over the years according to the presence of the TG or GG genotype (β=0.01, 95%CI: 0.01-0.02), particularly in females (β=0.02, 95%CI: 0.01-0.04). The ADIPOQ-rs2241766 TG and GG genotypes increased the risk of excess body weight in children from birth to six years of age and had a positive effect on body weight trajectories in girls. The LEP-rs7799039 genetic variant was not associated with body weight trajectory in children.

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“…However, in these studies, no direct evidence was obtained to support that paternal Zn status could attenuate ME intake and weight gain in female mice, which may be caused by the age and gender variance in mice ( Weigand and Egenolf, 2017 ). Moreover, it was reported that elevated leptin and abrogated adiponectin concentrations may reduce appetite and caloric intake ( Kroll et al., 2019 ), thus it could be inferred that increasing adiponectin and decreasing leptin concentrations may be considered to be a feedback regulation on the negative energy balance. A previous study also showed that paternal ZnD could induce a variety of metabolic abnormalities in liver ( Himoto and Masaki, 2018 ).…”

Section: Discussionmentioning

confidence: 99%

Paternal Zn-deficiency abolishes metabolic effects in offspring induced by diet type

Dong

Yue

et al. 2022

Animal Nutrition

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Accumulating evidence implicates that offspring are susceptible to paternal alterations in numerous fetal disorders, such as growth and metabolic defects. However, less study has been conducted to define the relationship between paternal zinc deficiency (ZnD) and energy metabolism of offspring. In the present study, we used a paternal ZnD exposure (Zn at 0.3 μg/g) model to test energy metabolism of male and female offspring with the intervention of diet type (high-fat diet and low-fat diet). Our results demonstrated that paternal ZnD decreased body weight (BW) gain per week ( P < 0.01) and ME intake per week ( P < 0.05) at 11 weeks in male offspring with high-fat diet intervention but not in female offspring. Further, anabolism and catabolism of hepatic energy products also exhibited alterations. ZnD attenuated liver glucose but increased lipids content accompanied with elevated adiponectin and reduction in leptin level in serum, which exhibited lipid metabolic disturbance and smaller ratio of liver weight to BW in male but not female offspring. The qRT-PCR and liver energy metabolites analysis revealed that paternal ZnD mainly induced reduction in glucose tolerance and lowered glucose uptaking ability in male offspring and thereby alleviated glycolysis and the tricarboxylic acid cycle (TCA) cycle, which displayed a male gender-dependency. Therefore, we propose that paternal ZnD abolishes metabolic effects in male offspring induced by diet type intervention. Our findings reveal a novel link between paternal Zn-D and offspring energy metabolism.

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Associations of ADIPOQ and LEP Gene Variants with Energy Intake: A Systematic Review

Cited by 14 publications

References 71 publications

Genetic polymorphisms and plasma concentrations of leptin (rs7799039) and adiponectin (rs17300539) are associated with obesity in children and adolescents

Genetic polymorphisms and plasma concentrations of leptin (rs7799039) and adiponectin (rs17300539) are associated with obesity in children and adolescents

Adiponectin and leptin gene variants and their effects on body weight trajectories in children from birth to 6 years of age: the PREDI Study

Paternal Zn-deficiency abolishes metabolic effects in offspring induced by diet type

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