Evidence that a maternal “junk food” diet during pregnancy and lactation can reduce muscle force in offspring

Bayol, Stephanie; Macharia, Raymond; Farrington, Samantha J.; Simbi, Bigboy H.; Stickland, N. C.

doi:10.1007/s00394-008-0760-5

Cited by 64 publications

(50 citation statements)

References 15 publications

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“…17 The maximal twitch tension and maximal tetanic tension of the semitendinosus are reduced in offspring of junk food-fed mothers. 29 When expressed relative to muscle mass, force production is decreased in the offspring of junk food-fed rats, regardless of weaning diet. Taken together, these results suggest that offspring of high fat fed/obese mothers have reduced muscle mass, and the muscle they do have are weaker than offspring of control-fed mothers.…”

Section: Discussionmentioning

confidence: 99%

A systematic review on animal models of maternal high fat feeding and offspring glycaemic control

et al. 2010

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The mechanistic link between obese parents and obese offspring and the relative role of genes, and a shared environment is not completely understood. Animal models help us to differentiate between genetic and environmental factors, and the interaction between the two. However, the willingness of researchers to blend results from multiple models makes it difficult for clear mechanisms to be identified for specific hypothesis-driven research. As such we conducted a systematic review of animal models of maternal high fat feeding in an effort to identify the affect on the offspring glycaemic control. Maternal and offspring outcomes are reported in an effort to identify possible relationships to facilitate and focus on future research. We present here data from 11 studies investigating glycaemic control in offspring exposed to a high fat diet (HFD) during maternal gestation only or gestation and lactation. Studies in this review identify a real risk of type 2 diabetes and obesity in male offspring exposed to a maternal HFD. Poor glycaemic control in the offspring appears to be independent of maternal obesity, birth weight or postweaning macronutrient intake. Inconsistencies between studies however, limit our capacity to identify mechanisms for the developmental origin of these diseases in animal models of overnutrition.

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Section: Discussionmentioning

confidence: 99%

A systematic review on animal models of maternal high fat feeding and offspring glycaemic control

et al. 2010

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“…The primary function of skeletal muscle is contraction-induced force production for movement. Bayol et al 65 showed that the maximal twitch tension and maximal tetanic tension of the semitendinosus were reduced in 10-week-old offspring of junk food fed mothers. This reduced muscle function was observed in offspring that were exposed to the junk food diet throughout gestation, lactation and post-weaning development, as well as offspring exposed to junk food diet during gestation and lactation only.…”

Section: Evidence For Reduced Energy Expenditure In the Offspring Of mentioning

confidence: 99%

Maternal over-nutrition and offspring obesity predisposition: targets for preventative interventions

Rooney

Ozanne

2011

Int J Obes

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Obesity now represents one of the major health care issues of the 21st century. Its prevalence has increased exponentially in both the developed and developing world during the last couple of decades. Such a rapid rise can therefore not be explained by a change in genotype, but must result from environmental factors and their interaction with our genes. There is clear evidence to show that current environmental factors such as current diet and level of physical activity can influence our risk of obesity. However, there is growing evidence to suggest that factors acting during very early life can influence long-term energy balance. One such factor that is emerging as an important player is maternal obesity and/or over-nutrition during pregnancy and lactation. Early life may therefore represent a critical period during which intervention strategies could be developed to reduce the prevalence of obesity.

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“…Activation of this pathway has been reported in inflammatory-related states of muscle atrophy and more recently in obesity-associated diseases (3). While there is some evidence regarding the impact of maternal HF diets on offspring skeletal muscle impairment (5,6,26,39), the role of intramuscular inflammation and associated catabolic pathways has not been comprehensively assessed.…”

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confidence: 99%

Maternal conjugated linoleic acid supplementation reverses high-fat diet-induced skeletal muscle atrophy and inflammation in adult male rat offspring

Pileggi

Segovia

Markworth

et al. 2016

American Journal of Physiology-Regulatory, Integrative and Comp

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-A high-saturated-fat diet (HFD) during pregnancy and lactation leads to metabolic disorders in offspring concomitant with increased adiposity and a proinflammatory phenotype in later life. During the fetal period, the impact of maternal diet on skeletal muscle development is poorly described, despite this tissue exerting a major influence on life-long metabolic health. This study investigated the effect of a maternal HFD on skeletal muscle anabolic, catabolic, and inflammatory signaling in adult rat offspring. Furthermore, the actions of maternal-supplemented conjugated linoleic acid (CLA) on these measures of muscle phenotype were investigated. A purified control diet (CD; 10% kcal fat), a CD supplemented with CLA (CLA; 10% kcal fat, 1% total fat as CLA), a high-fat (HFD; 45% kcal fat from lard), or a HFD supplemented with CLA (HFCLA; 45% kcal fat from lard, 1% total fat as CLA) was fed ad libitum to female Sprague-Dawley rats for 10 days before mating and throughout gestation and lactation. Male offspring received a standard chow diet from weaning, and the gastrocnemius was collected for analysis at day 150. Offspring from HF and HFCLA mothers displayed lower muscular protein content accompanied by elevated monocyte chemotactic protein-1, IL-6, and IL-1␤ concentrations. Phosphorylation of NF-Bp65 (Ser 536 ) and expression of the catabolic E3 ligase muscle ring finger 1 (MuRF1) were increased in HF offspring, an effect reversed by maternal CLA supplementation. The present study demonstrates the importance of early life interventions to ameliorate the negative effects of poor maternal diet on offspring skeletal muscle development. maternal obesity; nuclear factor-B

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Evidence that a maternal “junk food” diet during pregnancy and lactation can reduce muscle force in offspring

Abstract: Maternal malnutrition can influence muscle force production in offspring which may affect an individual's ability to exercise and thereby combat obesity.

Cited by 64 publications

References 15 publications

A systematic review on animal models of maternal high fat feeding and offspring glycaemic control

A systematic review on animal models of maternal high fat feeding and offspring glycaemic control

Maternal over-nutrition and offspring obesity predisposition: targets for preventative interventions

Maternal conjugated linoleic acid supplementation reverses high-fat diet-induced skeletal muscle atrophy and inflammation in adult male rat offspring

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