Essay on Animal and Cell Models for Human Nutrition

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Assignment
Animal and Cell Models for Human Nutrition

Table of contents

1. Discussion of study and the process being investigated………………………….3
1.1. Application to human studies……………………………………………3

2. What is known about the mechanisms involved? ………………………………..3

3. The approach and findings of the paper
3.1. Methods……………………………………………………………………4
3.2. Results.……………………………………………………………........….5
3.3. Findings……………………………………………………………………5

4. The different experimental models used to study this particular process
4.1 Animal models……………………………………………………………..6
4.1.1 Rodent models…………………………………………………….6
4.1.1.1 Mouse models…………………………………………….6
4.1.1.2 Rat models………………………………………………..7
4.1.2 Non-human primates models.……………………………………..8
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The aim of the study was in investigate whether long-term consumption of a high fat diet by the mother predisposes her offspring to enhanced susceptibility of developing features of the metabolic syndrome including hypertension and diabetes in later life (Elahi et al, 2009).

Application to human studies
This study demonstrates that maternal over-nutrition in rodents can increase the susceptibility of the offspring to features of the human metabolic syndrome (Elahi et al, 2009). The authors acknowledge that previous experimental studies were confined to short-term modification of the maternal diet during pregnancy and/or lactation periods. This present study involves a long-term dietary regimen and can be more applicable to human populations where consumption of high-fat foods occurs early in life and continues through to pregnancy and lactation (Elahi et al, 2009).

2. What is known about the mechanisms involved?

The thrifty phenotype hypothesis can be used to explain some of the mechanisms involved in this study (Williams et al, 2013). The development of the fetus relies on the nutritional intake received from the mother. Therefore, any changes in maternal metabolism would expose the fetus to a disturbed intrauterine environment that may subject the offspring to metabolic disease in later life (Williams et al, 2013). This concept is known as developmental origins of health and disease (DOHaD). This hypothesis focuses on the phase of

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