Effects of maternal high fat intake during pregnancy and lactation on total cholesterol and adipose tissue in neonatal rats

Lima, M. S.; Perez, G. S.; Morais, Graciele Lima; Santos, L. S.; Cordeiro, G. S.; Couto, Ricardo David; Deiró, T. C. B. J.; Leandro, Carol Góis; Barreto-Medeiros, Jairza Maria

doi:10.1590/1519-6984.166788

Cited by 13 publications

(6 citation statements)

References 17 publications

(17 reference statements)

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“…In addition, we found that pups from mothers fed a HFD had higher serum TC levels at 16 weeks old. Previous studies also found that serum TC levels were persistently higher in offspring from maternal HFD exposure than in those from maternal chow exposure at 3 weeks old (12,40). Moreover, our data showed that maternal HFD exposure led to an increase BAT weight in adult male offspring.…”

Section: Discussionsupporting

confidence: 77%

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Maternal High-Fat Diet Disturbs the DNA Methylation Profile in the Brown Adipose Tissue of Offspring Mice

et al. 2021

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The prevalence of obesity has become a threatening global public health issue. The consequence of obesity is abnormal energy metabolism. Unlike white adipose tissue (WAT), brown adipose tissue (BAT) has a unique role in nonshivering thermogenesis. Lipids and glucose are consumed to maintain energy and metabolic homeostasis in BAT. Recently, accumulating evidence has indicated that exposure to excess maternal energy intake affects energy metabolism in offspring throughout their life. However, whether excess intrauterine energy intake influences BAT metabolism in adulthood is not clear. In this study, mouse dams were exposed to excess energy intake by feeding a high-fat diet (HFD) before and during pregnancy and lactation. The histology of BAT was assessed by hematoxylin and eosin staining. The genome-wide methylation profile of BAT was determined by a DNA methylation array, and specific site DNA methylation was quantitatively analyzed by methylated DNA immunoprecipitation (MeDIP) qPCR. We found that intrauterine exposure to a high-energy diet resulted in blood lipid panel disorders and impaired the BAT structure. Higher methylation levels of genes involved in thermogenesis and fatty acid oxidation (FAO) in BAT, such as Acaa2, Acsl1, and Cox7a1, were found in 16-week-old offspring from mothers fed with HFD. Furthermore, the expression of Acaa2, Acsl1, and Cox7a1 was down-regulated by intrauterine exposure to excess energy intake. In summary, our results reveal that excess maternal energy leads to a long-term disorder of BAT in offspring that involves the activation of DNA methylation of BAT-specific genes involved in fatty acid oxidation and thermogenesis.

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Section: Discussionsupporting

confidence: 77%

“…BAT "whitening" is related to the progression of obesity. Activation of BAT is a potent target for metabolic diseases, such as diabetes and obesity (40,41).…”

Section: Discussionmentioning

confidence: 99%

Maternal High-Fat Diet Disturbs the DNA Methylation Profile in the Brown Adipose Tissue of Offspring Mice

et al. 2021

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“…This evidence explains why women with obesity breastfeed for a shorter duration and introduce complementary food earlier than women with normal weight [165]. Moreover, a study conducted by Lima et al in pregnant rats divided into two groups, one control and one fed with a HFD, showed that maternal lipids are reflected in milk composition, and a HFD leads to hypercholesterolemia and visceral fat accumulation in the offspring [166]. Maternal obesity is also associated with the alteration of immunological factor concentrations in human milk, such as C-reactive protein (CRP), leptin, IL-6, insulin, TNF-α, ghrelin, adiponectin, and obestatin.…”

Section: Impact Of Maternal Obesity On Pufa Metabolism During Breastfmentioning

confidence: 99%

Impact of Maternal Obesity on the Metabolism and Bioavailability of Polyunsaturated Fatty Acids during Pregnancy and Breastfeeding

et al. 2020

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Prenatal and postnatal development are closely related to healthy maternal conditions that allow for the provision of all nutritional requirements to the offspring. In this regard, an appropriate supply of fatty acids (FA), mainly n-3 and n-6 long-chain polyunsaturated fatty acids (LCPUFA), is crucial to ensure a normal development, because they are an integral part of cell membranes and participate in the synthesis of bioactive molecules that regulate multiple signaling pathways. On the other hand, maternal obesity and excessive gestational weight gain affect FA supply to the fetus and neonate, altering placental nutrient transfer, as well as the production and composition of breast milk during lactation. In this regard, maternal obesity modifies FA profile, resulting in low n-3 and elevated n-6 PUFA levels in maternal and fetal circulation during pregnancy, as well as in breast milk during lactation. These modifications are associated with a pro-inflammatory state and oxidative stress with short and long-term consequences in different organs of the fetus and neonate, including in the liver, brain, skeletal muscle, and adipose tissue. Altogether, these changes confer to the offspring a higher risk of developing obesity and its complications, as well as neuropsychiatric disorders, asthma, and cancer. Considering the consequences of an abnormal FA supply to offspring induced by maternal obesity, we aimed to review the effects of obesity on the metabolism and bioavailability of FA during pregnancy and breastfeeding, with an emphasis on LCPUFA homeostasis.

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“…Animal studies assessing the effect of maternal obesity/ obesogenic diets on offspring adiposity broadly seem to support human association data and show consistent outcomes across species (Table 3). Offspring from obese/highfat diet-fed mothers show increased adiposity [88][89][90] and adipocyte hypertrophy postnatally [89,91]. They also often show increased inflammatory marker expression and a higher infiltration of macrophages and other immune cells in their adipose tissue [89,91,92], which may reflect lipotoxicity and likely contributed to the glucose intolerance seen in such offspring.…”

Section: Maternal Obesity/obesogenic Diets and Offspring Adipositymentioning

confidence: 99%

Developmental programming of offspring adipose tissue biology and obesity risk

Rodgers

Sferruzzi‐Perri

2021

Int J Obes

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Obesity is reaching epidemic proportions and imposes major negative health crises and an economic burden in both high and low income countries. The multifaceted nature of obesity represents a major health challenge, with obesity affecting a variety of different organs and increases the risk of many other noncommunicable diseases, such as type 2 diabetes, fatty liver disease, dementia, cardiovascular diseases, and even cancer. The defining organ of obesity is the adipose tissue, highlighting the need to more comprehensively understand the development and biology of this tissue to understand the pathogenesis of obesity. Adipose tissue is a miscellaneous and highly plastic endocrine organ. It comes in many different sizes and shades and is distributed throughout many different locations in the body. Though its development begins prenatally, quite uniquely, it has the capacity for unlimited growth throughout adulthood. Adipose tissue is also a highly sexually dimorphic tissue, patterning men and women in different ways, which means the risks associated with obesity are also sexually dimorphic. Recent studies show that environmental factors during prenatal and early stages of postnatal development have the capacity to programme the structure and function of adipose tissue, with implications for the development of obesity. This review summarizes the evidence for a role for early environmental factors, such as maternal malnutrition, hypoxia, and exposure to excess hormones and endocrine disruptors during gestation in the programming of adipose tissue and obesity in the offspring. We will also discuss the complexity of studying adipose tissue biology and the importance of appreciating nuances in adipose tissue, such as sexual dimorphism and divergent responses to metabolic and endocrine stimuli. Given the rising levels of obesity worldwide, understanding how environmental conditions in early life affects adipose tissue phenotype and the subsequent development of obesity is of absolute importance.

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Effects of maternal high fat intake during pregnancy and lactation on total cholesterol and adipose tissue in neonatal rats

Cited by 13 publications

References 17 publications

Maternal High-Fat Diet Disturbs the DNA Methylation Profile in the Brown Adipose Tissue of Offspring Mice

Maternal High-Fat Diet Disturbs the DNA Methylation Profile in the Brown Adipose Tissue of Offspring Mice

Impact of Maternal Obesity on the Metabolism and Bioavailability of Polyunsaturated Fatty Acids during Pregnancy and Breastfeeding

Developmental programming of offspring adipose tissue biology and obesity risk

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