Early Nutrition and Later Obesity: Animal Models Provide Insights into Mechanisms

Metges, C. C.

doi:10.1007/978-1-4020-9173-5_11

Cited by 47 publications

(34 citation statements)

References 41 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In rodents, previous studies showed that alterations in leptin concentrations during the key perinatal periods of hypothalamic development may program selective leptin resistance (17). Neonatal leptin is required to the adequate development of hypothalamic arcuate nucleus and later functioning of hypothalamic circuits that control energy balance.…”

Section: Discussionmentioning

confidence: 99%

Sexual Dimorphism in the Early Life Programming of Serum Leptin Levels in European Adolescents: The HELENA Study

Labayen

Ruiz

Huybrechts

et al. 2011

The Journal of Clinical Endocrinology & Metabolism

View full text Add to dashboard Cite

show abstract

Section: Discussionmentioning

confidence: 99%

Sexual Dimorphism in the Early Life Programming of Serum Leptin Levels in European Adolescents: The HELENA Study

Labayen

Ruiz

Huybrechts

et al. 2011

The Journal of Clinical Endocrinology & Metabolism

View full text Add to dashboard Cite

show abstract

“…bacterial complement (Ozanne et al, 2004;Kotz, 2008;Pomp and Mohlke, 2008;Gluckman and Hanson, 2009;Metges, 2009). We also have strong evidence for genetic effects on aspects of eating behaviour in both humans and rodents (Koteja et al, 2003;de Castro, 2004;Rankinen and Bouchard, 2006;de Krom et al, 2009), and emerging evidence that in rodents and humans the propensity for physical activity and aspects of eating behaviour can be genetically related and possibly genetically correlated (Cai et al, 2006;Jonas et al, 2010a;Kumar et al, 2010).…”

Section: Genetic Basis Of Variation In Physical Activity and Related mentioning

confidence: 99%

The biological control of voluntary exercise, spontaneous physical activity and daily energy expenditure in relation to obesity: human and rodent perspectives

Garland

Schutz

Chappell

et al. 2011

Journal of Experimental Biology

376

434

View full text Add to dashboard Cite

Summary Mammals expend energy in many ways, including basic cellular maintenance and repair, digestion, thermoregulation, locomotion, growth and reproduction. These processes can vary tremendously among species and individuals, potentially leading to large variation in daily energy expenditure (DEE). Locomotor energy costs can be substantial for large-bodied species and those with high-activity lifestyles. For humans in industrialized societies, locomotion necessary for daily activities is often relatively low, so it has been presumed that activity energy expenditure and DEE are lower than in our ancestors. Whether this is true and has contributed to a rise in obesity is controversial. In humans, much attention has centered on spontaneous physical activity (SPA) or non-exercise activity thermogenesis (NEAT), the latter sometimes defined so broadly as to include all energy expended due to activity, exclusive of volitional exercise. Given that most people in Western societies engage in little voluntary exercise, increasing NEAT may be an effective way to maintain DEE and combat overweight and obesity. One way to promote NEAT is to decrease the amount of time spent on sedentary behaviours (e.g. watching television). The effects of voluntary exercise on other components of physical activity are highly variable in humans, partly as a function of age, and have rarely been studied in rodents. However, most rodent studies indicate that food consumption increases in the presence of wheels; therefore, other aspects of physical activity are not reduced enough to compensate for the energetic cost of wheel running. Most rodent studies also show negative effects of wheel access on body fat, especially in males. Sedentary behaviours per se have not been studied in rodents in relation to obesity. Several lines of evidence demonstrate the important role of dopamine, in addition to other neural signaling networks (e.g. the endocannabinoid system), in the control of voluntary exercise. A largely separate literature points to a key role for orexins in SPA and NEAT. Brain reward centers are involved in both types of physical activities and eating behaviours, likely leading to complex interactions. Moreover, voluntary exercise and, possibly, eating can be addictive. A growing body of research considers the relationships between personality traits and physical activity, appetite, obesity and other aspects of physical and mental health. Future studies should explore the neurobiology, endocrinology and genetics of physical activity and sedentary behaviour by examining key brain areas, neurotransmitters and hormones involved in motivation, reward and/or the regulation of energy balance.

show abstract

“…The main models are based in laboratory rodents, specially rats and mice [10,11], because they are relatively inexpensive to maintain, have a sequenced genome and are easily modified by genetic engineering. Thus, there are many studies on the fetal origin of diseases in rodents.…”

Section: Introductionmentioning

confidence: 99%

Genetic Basis, Nutritional Challenges and Adaptive Responses in the Prenatal Origin of Obesity and Type-2 Diabetes

González-Bulnes¹,

Óvilo²

2012

CDR

View full text Add to dashboard Cite

Obesity and type-2 diabetes are currently considered global pandemics. A large set of epidemiological evidences are addressing both the importance of a genetic predisposition -starting with the thrifty genotype hypothesis- and the determinant role of the maternal nutrition during pregnancy -starting with longitudinal studies of individuals born during the Dutch famine- on the adult onset of the disease. Compelling evidences suggest that both over- and undernutrition may modify the intrauterine environment of the conceptus and may alter the expression of its genome, predisposing to disease in the adult life. However, the most recent data indicate that the consequences of this phenomenon, termed as prenatal programming, are influenced both by timing, degree and duration of the challenge and by the adaptive response of the mother and the conceptus; thus, the information acquired by interventional studies modifying these parameters is becoming increasingly important. Obviously, interventional research in human beings is limited by ethical issues; hence, investigations need to be conducted on animal models, either rodents or large animals. This review summarizes the results of epidemiological human studies and translational animal research in unraveling the interaction between genome, nutritional status and adaptive response on the establishment of postnatal obesity, insulin resistance and type-2 diabetes.

show abstract

Early Nutrition and Later Obesity: Animal Models Provide Insights into Mechanisms

Cited by 47 publications

References 41 publications

Sexual Dimorphism in the Early Life Programming of Serum Leptin Levels in European Adolescents: The HELENA Study

Sexual Dimorphism in the Early Life Programming of Serum Leptin Levels in European Adolescents: The HELENA Study

The biological control of voluntary exercise, spontaneous physical activity and daily energy expenditure in relation to obesity: human and rodent perspectives

Genetic Basis, Nutritional Challenges and Adaptive Responses in the Prenatal Origin of Obesity and Type-2 Diabetes

Contact Info

Product

Resources

About