scholarly journals Maternal High-Fat Diet Modulates Cnr1 Gene Expression in Male Rat Offspring

Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2885
Author(s):  
Dawid Gawliński ◽  
Kinga Gawlińska ◽  
Irena Smaga

In recent years, strong evidence has emerged that exposure to a maternal high-fat diet (HFD) provokes changes in the structure, function, and development of the offspring’s brain and may induce several neurodevelopmental and psychiatric illnesses. The aims of this study were to evaluate the effects of a maternal HFD during pregnancy and lactation on depressive-like behavior and Cnr1 gene expression (encoding the CB1 receptor) in brain structures of rat offspring and to investigate the epigenetic mechanism involved in this gene expression. We found that a maternal HFD during pregnancy and lactation induced a depressive-like phenotype at postnatal days (PNDs) 28 and 63. We found that a maternal HFD decreased the Cnr1 mRNA levels in the prefrontal cortex with the increased levels of miR-212-5p and methylation of CpG islands at the Cnr1 promoter and reduced the level of Cnr1 gene expression in the dorsal striatum with an increased level of miR-154-3p in adolescent male offspring. A contrasting effect of a maternal HFD was observed in the hippocampus, where upregulation of Cnr1 gene expression was accompanied by a decrease of miR-154-3p (at PNDs 28 and 63) and miR-212-5p (at PND 63) expression and methylation of CpG islands at the Cnr1 promoter in male offspring. In summary, we showed that a maternal HFD during pregnancy and lactation triggered several epigenetic mechanisms in the brains of rat offspring, which may be related to long-lasting alterations in the next generation and produce behavioral changes in offspring, including a depressive-like phenotype.

Appetite ◽  
2011 ◽  
Vol 57 ◽  
pp. S15
Author(s):  
E.R. Ewald ◽  
B. Sun ◽  
R.H. Purcell ◽  
R.S. Lee ◽  
J.B. Potash ◽  
...  

2012 ◽  
Vol 2012 ◽  
pp. 1-10 ◽  
Author(s):  
J. Beltrand ◽  
D. M. Sloboda ◽  
K. L. Connor ◽  
M. Truong ◽  
M. H. Vickers

Epidemiological and experimental studies report associations between overweight mothers and increased obesity risk in offspring. It is unclear whether neonatal leptin regulation mediates this association between overweight mothers and offspring obesity. We investigated the effect of neonatal treatment with a leptin antagonist (LA) on growth and metabolism in offspring of mothers fed either a control or a high fat diet. Wistar rats were fed either a control (CON) or a high fat diet (MHF) during pregnancy and lactation. Male CON and MHF neonates received either saline (S) or a rat-specific pegylated LA on days 3, 5, and 7. Offspring were weaned onto either a control or a high fat (hf) diet. At day 100, body composition, blood glucose,β-hydroxybutyrate and plasma leptin and insulin were determined. In CON and MHF offspring, LA increased neonatal bodyweights compared to saline-treated offspring and was more pronounced in MHF offspring. In the post-weaning period, neonatal LA treatment decreased hf diet-induced weight gain but only in CON offspring. LA treatment induced changes in body length, fat mass, body temperature, and bone composition. Neonatal LA treatment can therefore exert effects on growth and metabolism in adulthood but is dependent upon interactions between maternal and post-weaning nutrition.


2019 ◽  
Author(s):  
Sanoji Wijenayake ◽  
Mouly F. Rahman ◽  
Christine M.W. Lum ◽  
Wilfred C. De Vega ◽  
Aya Sasaki ◽  
...  

ABSTRACTBackgroundAcute elevations in endogenous corticosterone (CORT) with psychosocial stress or exogenous administration potentiate inflammatory gene expression. Maternal obesity as a result of high-fat diet (HFD) consumption has been linked to higher basal levels of neuroinflammation, including increased expression of pro-inflammatory genes in the amygdala. These findings suggest that exposure to maternal HFD may elicit pro-inflammatory responses in the presence of an immune stressor such as lipopolysaccharide (LPS), a component of gram-negative bacteria, as well as acute elevated CORT.MethodsRat offspring were exposed to maternal HFD or control diet (CHD) throughout pre and postnatal development until weaning, when all offspring were provided CHD until adulthood. In adulthood, offspring were ‘challenged’ with administration of exogenous CORT, to simulate an acute physiological stress, LPS, to induce an immune stress, or both. qPCR was used to measure transcript abundance of CORT receptors and downstream inflammatory genes in the amygdala, hippocampus and prefrontal cortex, brain regions that mediate neuroendocrine and behavioral responses to stress.ResultsHFD female offspring exhibited elevations in anti-inflammatory transcripts, whereas HFD male offspring responded with greater pro-inflammatory gene expression to simultaneous CORT and LPS administration.ConclusionsThese findings suggest that exposure to maternal HFD leads to sex-specific alterations that may alter inflammatory responses in the brain, possibly as an adaptive response to basal inflammation.


2019 ◽  
Vol 318 ◽  
pp. 92-100 ◽  
Author(s):  
Zachary A. Cordner ◽  
Seva G. Khambadkone ◽  
Gretha J. Boersma ◽  
Lin Song ◽  
Tyler N. Summers ◽  
...  

2021 ◽  
pp. 1-15

Maternal lifestyle influence may be a factor in the worldwide prevalence of obesity and its complications, including diabetes. Studies investigating the effect of the perinatal maternal environment have produced a range of results, sometimes diametrically opposite. The present study was designed to investigate how obesity and weight gain in pregnant mice affects energy balance, body composition and glucose homeostasis in their offspring, both at a young age on standard diet and when older and fed a high-fat diet. At six weeks of age both male and female offspring from mothers fed a high fat diet had a shorter body length than those from mothers fed standard chow. In contrast to males, female offspring also contained a higher proportion of fat and had elevated circulating leptin and adiponectin. Their gonadal fat pads were heavier and contained larger adipocytes, whereas male offspring had proportionally more smaller adipocytes. Six-week-old female, but not male, offspring had increased gonadal fat gene expression of acetyl CoA carboxylase 1, the rate-limiting step in lipid biosynthesis, and decreased gene expression of carnitine palmitoyl transferase 1, the rate-limiting step in fatty acid oxidation. Maternal high fat diet had no effect on glucose tolerance in six-week-old mice, but this was achieved with higher insulin levels in females. Contrastingly, when the offspring were fed a high fat diet for three months, female, but not male, offspring were leaner than those from mothers fed standard chow. Their gonadal fat depots were lighter and the adipocytes were smaller. Female, but not male, offspring fed high fat diet had decreased gonadal fat gene expression of acetyl CoA carboxylase 1, and increased gene expression of carnitine palmitoyl transferase 1. High fat diet-induced glucose intolerance and elevated plasma insulin concentration were improved in female, but not male, offspring. Plasma leptin and adiponectin remained higher in female offspring on high fat diet with resistin levels being lower. These results suggest that the gonadal fat of female offspring is more adaptable to different levels of dietary fat exposure, increasing storage when levels are low and increasing oxidation when levels are high. This may help female offspring be more resistant to the detrimental effects of high fat diet than male mice.


2015 ◽  
Vol 6 ◽  
Author(s):  
You-Lin Tain ◽  
Jiunn-Ming Sheen ◽  
Hong-Ren Yu ◽  
Chih-Cheng Chen ◽  
Mao-Meng Tiao ◽  
...  

Diabetes ◽  
2015 ◽  
Vol 65 (3) ◽  
pp. 574-584 ◽  
Author(s):  
Michael Kruse ◽  
Farnaz Keyhani-Nejad ◽  
Frank Isken ◽  
Barbara Nitz ◽  
Anja Kretschmer ◽  
...  

2022 ◽  
Vol 82 ◽  
Author(s):  
L. S. Santos ◽  
R. J. B. Matos ◽  
G. S. Cordeiro ◽  
G. S. Perez ◽  
D. A. E. Santo ◽  
...  

Abstract Exposure to the hight-fat diet may alter the control of food intake promoting hyperphagia and obesity. The objective of this study was to investigate the effects of this diet on dopamine receptors (drd1 and drd2), proopiomelanocortin (pomc), neuropeptideY (npy) genes expression, and preference food in adult rats. Wistar female rats were fed a hight-fat or control diet during pregnancy and lactation. The offspring were allocated into groups: Lactation – Control (C) and High-fat (H). Post-weaning – Control Control (CC), offspring of mothers C, fed a control diet after weaning; Control Hight-fat (CH), offspring of mothers C, fed a hight-fat diet after weaning; Hight-fat Control (HC), offspring of mothers H, fed with control diet after weaning; and Hight-fat Hight-fat (HH), offspring of mothers H, fed a H diet after weaning. The groups CH and HH presented greater expression of drd1 in comparison to the CC. The drd2 of CH and HC presented higher gene expression than did CC. HH presented higher pomc expression in comparison to the other groups. HC also presented greater expression in comparison to CH. The npy of HH presented greater expression in relation to CH and HC. HH and HC have had a higher preference for a high-fat diet at 102º life’s day. The high-fat diet altered the gene expression of the drd1, drd2, pomc and npy, and influencing the food preference for high-fat diet.


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