Obesity as the Sequel of Childhood Stunting: Ghrelin and GHSR Gene Polymorphism Explained
Stunting or short stature in children is a significant nutritional problem in developing and underdeveloped countries. Stunting during childhood might affect brain development and impair development cognitive function. Additionally, this condition associated with the increased risk for obesity durin...
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| Language: | English |
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Interna Publishing
2018-06-01
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| Series: | Acta Medica Indonesiana |
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| Online Access: | https://actamedindones.org/index.php/ijim/article/view/493 |
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| author | Harry Freitag Luglio Muhammad |
| author_facet | Harry Freitag Luglio Muhammad |
| author_sort | Harry Freitag Luglio Muhammad |
| collection | DOAJ |
| description | Stunting or short stature in children is a significant nutritional problem in developing and underdeveloped countries. Stunting during childhood might affect brain development and impair development cognitive function. Additionally, this condition associated with the increased risk for obesity during adulthood. Several studies have shown that the increment risk of obesity and overweight in children with a short stature was due to their metabolic efficiency. Children with stunting have lower resting energy expenditure compared to non stunting children. Additionally, stunted children has higher respiratory quotient and carbohydrate oxidation but lower fat oxidation compared to non-stunting children. These results might explain why stunted children easily become obese, which is due to lower fat oxidation and leading to tendency to store fat.
This review discussed the current status on studies in the nutrigenetic aspects of the relationship between stunting in the childhood and obesity in adulthood. I hypothesized that stunted children are more likely to become obese in their later life because they have lower metabolic rate and higher tendency of fat storage. There are several candidate genes and pathway involved in obesity and I suspected that ghrelin and its receptor growth hormone secretague receptor (GHSR) were responsible.
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| format | Article |
| id | doaj-art-67df1d6972be4921b5da4f659bcaad5e |
| institution | DOAJ |
| issn | 0125-9326 2338-2732 |
| language | English |
| publishDate | 2018-06-01 |
| publisher | Interna Publishing |
| record_format | Article |
| series | Acta Medica Indonesiana |
| spelling | doaj-art-67df1d6972be4921b5da4f659bcaad5e2025-08-20T03:13:54ZengInterna PublishingActa Medica Indonesiana0125-93262338-27322018-06-01502260Obesity as the Sequel of Childhood Stunting: Ghrelin and GHSR Gene Polymorphism ExplainedHarry Freitag Luglio Muhammad0Department of Nutrition and Health, Faculty of Medicine, Public Health and Nursing, Universitas Gadjah Mada, Yogyakarta, IndonesiaStunting or short stature in children is a significant nutritional problem in developing and underdeveloped countries. Stunting during childhood might affect brain development and impair development cognitive function. Additionally, this condition associated with the increased risk for obesity during adulthood. Several studies have shown that the increment risk of obesity and overweight in children with a short stature was due to their metabolic efficiency. Children with stunting have lower resting energy expenditure compared to non stunting children. Additionally, stunted children has higher respiratory quotient and carbohydrate oxidation but lower fat oxidation compared to non-stunting children. These results might explain why stunted children easily become obese, which is due to lower fat oxidation and leading to tendency to store fat. This review discussed the current status on studies in the nutrigenetic aspects of the relationship between stunting in the childhood and obesity in adulthood. I hypothesized that stunted children are more likely to become obese in their later life because they have lower metabolic rate and higher tendency of fat storage. There are several candidate genes and pathway involved in obesity and I suspected that ghrelin and its receptor growth hormone secretague receptor (GHSR) were responsible. https://actamedindones.org/index.php/ijim/article/view/493stuntingobesityghrelingrowth hormone secretague receptor (GHSR)gene polymorphism |
| spellingShingle | Harry Freitag Luglio Muhammad Obesity as the Sequel of Childhood Stunting: Ghrelin and GHSR Gene Polymorphism Explained Acta Medica Indonesiana stunting obesity ghrelin growth hormone secretague receptor (GHSR) gene polymorphism |
| title | Obesity as the Sequel of Childhood Stunting: Ghrelin and GHSR Gene Polymorphism Explained |
| title_full | Obesity as the Sequel of Childhood Stunting: Ghrelin and GHSR Gene Polymorphism Explained |
| title_fullStr | Obesity as the Sequel of Childhood Stunting: Ghrelin and GHSR Gene Polymorphism Explained |
| title_full_unstemmed | Obesity as the Sequel of Childhood Stunting: Ghrelin and GHSR Gene Polymorphism Explained |
| title_short | Obesity as the Sequel of Childhood Stunting: Ghrelin and GHSR Gene Polymorphism Explained |
| title_sort | obesity as the sequel of childhood stunting ghrelin and ghsr gene polymorphism explained |
| topic | stunting obesity ghrelin growth hormone secretague receptor (GHSR) gene polymorphism |
| url | https://actamedindones.org/index.php/ijim/article/view/493 |
| work_keys_str_mv | AT harryfreitaglugliomuhammad obesityasthesequelofchildhoodstuntingghrelinandghsrgenepolymorphismexplained |