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      On the origin of obesity: identifying the biological, environmental and cultural drivers of genetic risk among human populations : Evolution and genetic risk of obesity

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          Obesity

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            Diet and the evolution of human amylase gene copy number variation.

            Starch consumption is a prominent characteristic of agricultural societies and hunter-gatherers in arid environments. In contrast, rainforest and circum-arctic hunter-gatherers and some pastoralists consume much less starch. This behavioral variation raises the possibility that different selective pressures have acted on amylase, the enzyme responsible for starch hydrolysis. We found that copy number of the salivary amylase gene (AMY1) is correlated positively with salivary amylase protein level and that individuals from populations with high-starch diets have, on average, more AMY1 copies than those with traditionally low-starch diets. Comparisons with other loci in a subset of these populations suggest that the extent of AMY1 copy number differentiation is highly unusual. This example of positive selection on a copy number-variable gene is, to our knowledge, one of the first discovered in the human genome. Higher AMY1 copy numbers and protein levels probably improve the digestion of starchy foods and may buffer against the fitness-reducing effects of intestinal disease.
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              A mutation in the human leptin receptor gene causes obesity and pituitary dysfunction.

              The adipocyte-specific hormone leptin, the product of the obese (ob) gene, regulates adipose-tissue mass through hypothalamic effects on satiety and energy expenditure. Leptin acts through the leptin receptor, a single-transmembrane-domain receptor of the cytokine-receptor family. In rodents, homozygous mutations in genes encoding leptin or the leptin receptor cause early-onset morbid obesity, hyperphagia and reduced energy expenditure. These rodents also show hypercortisolaemia, alterations in glucose homeostasis, dyslipidaemia, and infertility due to hypogonadotropic hypogonadisms. In humans, leptin deficiency due to a mutation in the leptin gene is associated with early-onset obesity. Here we describe a homozygous mutation in the human leptin receptor gene that results in a truncated leptin receptor lacking both the transmembrane and the intracellular domains. In addition to their early-onset morbid obesity, patients homozygous for this mutation have no pubertal development and their secretion of growth hormone and thyrotropin is reduced. These results indicate that leptin is an important physiological regulator of several endocrine functions in humans.
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                Author and article information

                Journal
                Obesity Reviews
                Obesity Reviews
                Wiley
                14677881
                February 2018
                February 2018
                November 16 2017
                : 19
                : 2
                : 121-149
                Affiliations
                [1 ]Department of Health Research Methods, Evidence, and Impact; McMaster University; Hamilton ON Canada
                [2 ]Department of Pediatrics; McMaster University; Hamilton ON Canada
                [3 ]Division of Pediatric Endocrinology; McMaster Children's Hospital; Hamilton ON Canada
                [4 ]Department of Biology; McMaster University; Hamilton ON Canada
                [5 ]Agent-Based Modelling Laboratory; York University; Toronto ON Canada
                [6 ]Institute of Biological and Environmental Sciences; University of Aberdeen; Aberdeen UK
                [7 ]State Key Laboratory of Molecular Developmental Biology, Institute of Genetics and Developmental Biology; Chinese Academy of Sciences; Beijing China
                [8 ]Department of Pathology and Molecular Medicine; McMaster University; Hamilton ON Canada
                Article
                10.1111/obr.12625
                © 2017

                http://doi.wiley.com/10.1002/tdm_license_1.1

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