scholarly journals Maternal Vitamin a Supplementation Modulates Adipose Tissue Development in Offspring of Rats Consuming a High-Fat Diet (FS06-02-19)

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Shu Hang Kwan ◽  
Katelyn Senkus ◽  
Kristi Crowe-White ◽  
Libo Tan

Abstract Objectives Vitamin A (VA) is a key regulator of obesity development and associated metabolic complications in adults. The aim of this study is to assess the impacts of VA supplementation during suckling and post-weaning periods on the adipose tissue (AT) development in rats reared by mothers consuming a high-fat diet (HFD). Methods Four Sprague-Dawley rats arrived on their 2nd day of gestation. After 3 days of acclimation, they were randomized to either a normal-fat diet (NFD = 25% fat) with adequate VA at 2.6 mg/kg (n = 2) or a HFD (50% fat) with the same amount of VA (n = 2). Upon delivery, pups were transferred to achieve a same number of n = 11/litter. Two mother rats, one from each group, were switched to a NFD and a HFD both with supplemented VA at 129 mg/kg (NFD + VA and HFD + VA), respectively. The other two remained on their diets with adequate VA through lactation (NFD and HFD). At postnatal day 14 (P14) and P25, 4 pups/litter were euthanized with body weight (BW), visceral white AT (WAT) mass, and brown AT (BAT) mass recorded. Serum samples from P25 necropsy were analyzed for glucose, lipids, leptin, adiponectin, and inflammatory biomarkers. At P25, the rest weanling pups (n = 3/group) were fed the diets as their respective mothers until they were euthanized at P35. Results At P14 and P25, the BW and WAT mass of pups in the HFD group were significantly (P < 0.05) higher than those in the NFD groups. Comparatively, these measures were significantly reduced in the HFD + VA group as compared to the HFD litter. A similar pattern of change in WAT mass was observed at P35. Additionally, at P25, the BAT mass of pups was significantly reduced by the maternal HFD, but VA supplement restored the level to that in the NFD groups. Serum analysis from P25 revealed a significantly higher adiponectin level in the HFD + VA group. In contrast, VA supplement showed a trend to reduce the glucose and leptin levels that were raised by the maternal HFD consumption. Conclusions Results support a regulatory role of VA supplementation during suckling and post-weaning period in the AT development in offspring from mothers consuming a HFD as evidenced by reduced BW and WAT mass, increased BAT mass, and modulation of adipokines. Future analysis will be conducted to study the mechanisms by which VA may impact the adipogenesis, WAT browning, and AT secretory functions. Funding Sources NIH.

2019 ◽  
Vol 3 (Supplement_1) ◽  
Author(s):  
Katelyn Senkus ◽  
Shu Hang Kwan ◽  
Libo Tan ◽  
Kristi Crowe-White

Abstract Objectives Excess adipose tissue (AT) may undergo adipocyte differentiation in response to nutritional stimuli. It is unknown if lycopene may metabolically activate adaptive thermogenesis and disrupt the ensuing dysfunction of an excessive energy burden. The purpose of this study was to assess AT development and metabolic profiles of Sprague-Dawley offspring from mothers fed high fat diets (HFD = 50% fat) supplemented with 1% lycopene during the suckling and post-weaning period. Methods Three Sprague-Dawley rats arrived on their 2nd day of gestation, and after three days of acclimation, mothers were randomized to a 25% normal-fat diet (NFD) or HFD. Upon delivery, one of the HFD mothers was transitioned to a HFD supplemented with 1% lycopene. Four pups/litter were euthanized at postnatal day 14 and 25 (P14 and P25, respectively) with body weight (BW) as well as the mass of visceral white AT (WAT) and brown AT (BAT) recorded. Serum samples from the P25 necropsy were analyzed for glucose, lipids, leptin, adiponectin, and inflammatory biomarkers. At P25, the remaining weanling pups (3 pups/litter) were fed the diets of their respective mothers until euthanizing at postnatal week 5 (P35). Results The HFD was effective in inducing weight gain as evidenced by increases in BW and WAT in the HFD group not receiving lycopene supplementation compared to pups from the NFD litter across all time points. At P14, WAT was 42.5% lower (P = 0.003) in rats reared by mothers consuming lycopene-supplemented HFD compared to the non-supplemented HFD group. At P25, significant decreases in WAT (P = 0.004, 25.6% lower) were also observed concomitantly with significant increases in BAT (P = 0.025, 40% increase) in rats reared by mothers consuming lycopene-supplemented HFD compared to the HFD group not receiving lycopene. Furthermore, at P25, glucose was 24% lower (P = 0.004) in the lycopene-supplemented HFD group. Albeit non-significant, BW and WAT in the lycopene-supplemented HFD group remained lower while BAT remained higher through P35. Conclusions Results suggest that lycopene may influence cardiometabolic outcomes such as accrual of AT mass and, subsequent obesity, as well as blood glucose dynamics. Additional research is warranted to determine diet-induced signaling pathways by which lycopene may influence adipocyte differentiation. Funding Sources NIH; University of Alabama Pilot Grant.


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 470-470
Author(s):  
Katelyn Senkus ◽  
Yanqi Zhang ◽  
Libo Tan ◽  
Kristi Crowe-White

Abstract Objectives Dietary patterns high in fat contribute to the onset of cardiometabolic disease through accrual of adipose tissue (AT). Nevertheless, carotenoids, such as lycopene, may disrupt these metabolic perturbations. The purpose of this study was to evaluate AT development, systemic and AT redox status, and cardiometabolic biomarkers during weaning and post-weaning periods of offspring from mothers fed high fat diets with and without lycopene supplementation. Methods Sprague-Dawley rats arrived on the 2nd day of gestation and were randomized to 25% normal fat diet (NFD) or 50% high fat diet (HFD). Upon delivery, half of HFD mothers were transitioned to HFD supplemented with 1% lycopene (HFDL group). Remaining mothers continued NFD or HFD without supplementation. Four pups/litter were euthanized at postnatal day 25 (P25). Beginning at P25, weanling pups were fed diets of their respective mothers until euthanization at P35 (three pups/litter). Visceral white AT (WAT) and brown AT (BAT) mass was determined, as well as lipid peroxides and antioxidant capacity (AC) of these tissues and serum. Cardiometabolic biomarkers were assessed at P25. Results At each time point, HFD groups had significantly greater (P &lt; 0.05) WAT accrual compared to NFD group, sufficiently representing diet-induced obesity. Compared to the HFD group, the HFDL group exhibited significantly greater BAT at P25 (P = 0.025) with a significant reduction in WAT mass (P = 0.004). Such patterns continued into P35, albeit non-significant. At both time points, serum lipid peroxides were significantly lower in the HFDL group compared to the HFD (P = 0.005, P = 0.003, respectively). In contrast, AT results were starkly different such that the HFDL group exhibited significantly greater (P &lt; 0.05) lipid peroxides in WAT and BAT at P25 and P35 compared to HFD group. No significant differences in systemic or AT AC were observed between groups. Furthermore, serum adiponectin and leptin did not differ significantly between groups despite the aforementioned modifications in AT development. Conclusions Results from this exploratory analysis suggest that lycopene may induce favorable alterations in AT development, yet it differentially influences redox status in serum and AT. Additional research is warranted to elucidate molecular mechanisms by which lycopene influences AT biology and redox status. Funding Sources NIH.


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 135-135
Author(s):  
Yanqi Zhang ◽  
Katelyn Senkus ◽  
Kristi Crowe-White ◽  
Libo Tan

Abstract Objectives Dietary fat can contribute to oxidative stress and adipose tissue (AT) accrual which exacerbates redox imbalance. Vitamin A (VA) has been shown to regulate AT development and associated metabolic conditions in adult models; however, such effects of VA in early life stages, especially on redox status, has barely been studied. The aim of this study was to assess the effects of VA supplementation during suckling and post-weaning periods on systemic and AT redox status in rats reared by mothers consuming a high-fat diet (HFD). Methods Sprague-Dawley rats arrived on their second day of gestation and were randomized to either a normal-fat diet (NFD = 25% fat) or a HFD (50% fat) both with adequate VA at 2.6 mg/kg. Upon delivery of pups, half of rat mothers from the NFD cohort or HFD cohort were switched to a NFD or a HFD both with supplemented VA at 129 mg/kg (NFD + VA and HFD + VA group), respectively. The other half of mothers remained on their diets with adequate VA (NFD and HFD group). At postnatal day 14 (P14), P25, and P35, pups (n = 4 or 3/group/time point) were euthanized. Concentrations of VA, lipid peroxides, and antioxidant capacity (AC) of serum, visceral white AT (WAT) and brown AT (BAT) were measured. Results At all three time points, the lipid peroxides concentration in WAT was significantly lower in VA-supplemented groups as compared to their respective control (P &lt; 0.0001 for NFD + VA vs. NFD; P &lt; 0.05 for HFD + VA vs. HFD); lipid peroxides were significantly (P &lt; 0.01) higher in the HFD + VA group than in the NFD + VA group. A significantly (P &lt; 0.05) positive correlation between the amount of VA and the lipophilic AC of the WAT was noted. For BAT, the NFD + VA group showed a significantly (P &lt; 0.001) lower lipid peroxides concentration as compared to the NFD group. However, such effect was not observed in the HFD cohort. Serum lipid peroxides in the HFD + VA group were significantly (P &lt; 0.05) lower than in the HFD group. A significant (P &lt; 0.0001) negative correlation was found between the serum concentration of VA and lipid peroxides. Conclusions VA supplementation during suckling and post-weaning period improved both the systemic and WAT redox status of rats reared by mothers consuming a HFD, as well as the status within both WAT and BAT of pups nursed by mothers consuming a NFD. The differing results in WAT and BAT may suggest their different roles in redox biology. Funding Sources NIH


2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 131-131
Author(s):  
Libo Tan ◽  
Hui Wang ◽  
Yanqi Zhang

Abstract Objectives Retinoic acid (RA), the active metabolite of vitamin A, has been shown to be a regulator of adipose tissue (AT) development in adult models. The aim of the study was to assess the effects of repeated RA treatments on body weight (BW) gain, AT development, and metabolic conditions of neonatal rats reared by mothers consuming a high-fat diet (HFD). Methods Five Sprague-Dawley rats arrived on their second day of gestation and were randomized to either a normal-fat diet (NFD = 25% fat; n = 2) or a HFD (50% fat; n = 3) both with a marginal level of VA at 0.35 mg/kg. Half of the pups delivered by mothers in HFD cohort received oral RA treatments. Specifically, on postnatal day 5 (P5) and P8, respectively, n = 12 pups in HFD cohort received an oral RA dose at 4 μg/g BW (HFD + RA group). Remaining pups in HFD cohort (n = 12; HFD group) and pups in NFD cohort (n = 12; NFD group) both received oil as placebo. Six hours after the dose administration on P8, n = 4 pups/group were euthanized with blood, visceral white AT (WAT), and brown AT (BAT) collected. On P11 and P14, remaining pups in NFD, HFD, and HFD + RA group (n = 8/group) received a dose of oil, oil, and RA, respectively. Six hours after the administration on P14, n = 4 pups/group were sacrificed. On P17 and P20, remaining pups in each group (n = 4) received their respective treatment and were euthanized six hours afterwards on P20. Serum samples from P14 and P20 sacrifice were analyzed for concentrations of glucose, insulin, lipids, adipokines, and inflammatory markers. Results At P8 and P14, no significant difference in BW gain, WAT mass, and BAT mass of pups was noted among groups. At P20, all three measures were significantly (P &lt; 0.05) higher in the HFD group than in the NFD group; the measures were significantly decreased in the HFD + RA group compared to the HFD group. At P20, serum adiponectin and leptin concentrations were both significantly higher in the HFD than in the NFD group; RA treatment significantly reduced the concentrations of both. The pattern of changes in serum leptin was also observed at P14. At both P14 and P20, serum triglyceride was found to be significantly higher in pups receiving RA treatment. Conclusions Repeated RA treatments exerted a regulatory role on the AT metabolism and development of neonatal offspring to mothers consuming a HFD, as evidenced by reduced BW gain and AT mass as well as modulation of adipokines. Funding Sources NIH.


2006 ◽  
Vol 76 (5) ◽  
pp. 271-279 ◽  
Author(s):  
Pérez de Heredia ◽  
Garaulet ◽  
Puy Portillo ◽  
Zamora

Susceptibility to dietary obesity was studied in Wistar and Sprague-Dawley rats submitted to different high-energy diets. Experiment 1: female Sprague-Dawley rats were fed chow (n = 6) or a high-fat diet (n = 12) for 22 weeks. Experiment 2: Wistar rats were fed chow or a high-fat diet, and Sprague-Dawley rats were given chow, high-fat, sweet condensed milk, or cafeteria diets, for eight weeks (6 animals per group). Food intake and body weight were recorded weekly. Adipose tissue was collected from periovarian, mesenteric, and subcutaneous regions and adipocytes were isolated and measured. Both strains showed similar energy intake and body weight gain. Wistar rats reached greater final body fat contents than Sprague-Dawley rats, regardless of the type of diet. However, resistance to dietary obesity was found in 100% of cases in both experiments. None of the diets succeeded in increasing body fat accumulation when compared to control groups. All adipose tissue locations were equally unaffected, with periovarian fat cells being larger than those in mesenteric and subcutaneous regions in all the groups. In view of the strong resistance to obesity observed in rats, it should be important for researchers to transmit the difficulties of inducing dietary obesity in these animals, in order to prevent bias in science interpretation.


2020 ◽  
Vol 4 (8) ◽  
Author(s):  
Libo Tan ◽  
Yanqi Zhang ◽  
Kristi M Crowe-White ◽  
Katelyn E Senkus ◽  
Maddy E Erwin ◽  
...  

ABSTRACT Background Vitamin A (VA) has been demonstrated to be a regulator of adipose tissue (AT) development in adult obese models. However, little is known about the effect of VA on obesity-associated developmental and metabolic conditions in early life. Objectives We aimed to assess the effects of dietary VA supplementation during suckling and postweaning periods on the adiposity and metabolic health of neonatal and weanling rats from mothers consuming a high-fat diet (HFD). Methods Pregnant Sprague-Dawley rats were fed a normal-fat diet (NFD; 25% fat; n = 2) or an HFD (50% fat; n = 2), both with 2.6 mg VA/kg. Upon delivery, half of the rat mothers were switched to diets with supplemented VA at 129 mg/kg, whereas the other half remained at 2.6 mg VA/kg. Four groups of rat pups were designated as NFD, NFD + VA, HFD, and HFD + VA, respectively. At postnatal day (P)14, P25, and P35, pups (n = 4 or 3/group) were killed. Body weight (BW), visceral white AT (WAT) mass, brown AT (BAT) mass, uncoupling protein 1 mRNA expression in BAT, serum glucose, lipids, adipokines, and inflammatory biomarkers, as well as serum and AT redox status were assessed. Results Rat pups in the HFD group exhibited significantly higher BW, WAT mass, and serum glucose and leptin but reduced BAT mass compared with the NFD group. Without affecting the dietary intake, supplementing the HFD with VA significantly reduced the BW and WAT mass of pups but increased the BAT mass, significantly lowered the systemic and WAT oxidative stress, and modulated serum adipokines and lipids to some extent. Conclusions VA supplementation during suckling and postweaning periods attenuated metabolic perturbations caused by excessive fat intake. Supplementing maternal or infant obesogenic diets with VA or establishing a higher RDA of VA for specific populations should be studied further for managing overweight/obesity in early life.


2020 ◽  
Author(s):  
Neng Tine Kartinah ◽  
Nisa Komara ◽  
Nuraini Diah Noviati ◽  
Syarifah Dewi ◽  
Sophie Yolanda ◽  
...  

Abstract Background Obesity is a cause of Fgf21 resistance, which affects the browning and thermogenesis process of the adipose tissue. Decreased receptor expression is influenced by microRNA 34a (miR-34a), whose expression is increased in obesity. While Fgf21-based therapies have been widely investigated, the potential activity of Hibiscus sabdariffa Linn extract (HSE) against Fgf21 resistance is unknown. This study aims to determine the effects of HSE on the expression of miR-34a and Fgf21 receptors in white adipose tissue. Methods This experimental study used 24 male Sprague-Dawley rats and divided into four groups: Control (N); diet-induced-obesity rats (DIO); DIO rats with HSE 200 mg/kgBW/day and DIO rats with HSE 400 mg/kgBW/day. Rats were fed a high-fat diet for 17 weeks. HSE was administered daily for five weeks. The administration of HSE 400 mg/kg BW/day resulted in the equivalent expression of miR-34a to that of the control (p > 0.05). Results Fgfr1 receptor expression was also similar to controls (p > 0.05). Beta-klotho expression was significantly lower than that of Control (p < 0.05) but equivalent to that of DIO rats (p < 0.05). Conclusions H. sabdariffa has the potential to reduce Fgf21 resistance in DIO rats through the suppression of miR-34a expression and an increase in the number of Fgfr1 and beta-klotho receptors in adipose tissue.


Metabolism ◽  
2021 ◽  
Vol 116 ◽  
pp. 154497
Author(s):  
Elif Günalan ◽  
Meyli Ezgi Karagöz ◽  
Bayram Yılmaz ◽  
Burcu Gemici

2013 ◽  
Vol 33 (suppl_1) ◽  
Author(s):  
Michael J Duryee ◽  
Anand Dusad ◽  
Scott W Shurmur ◽  
Michael D Johnston ◽  
Robert P Garvin ◽  
...  

Introduction Malondialdehyde/Acetaldehyde (MAA) modified proteins have been suggested to play a role in the development/progression of atherosclerosis. Circulating antibodies directed against these proteins have recently been shown to be associated with the severity of the disease. More specifically, the isotype of the antibody to MAA correlated with either an acute MI (IgG) or stable plaque formation (IgA) formation. MAA is thought to form as a result of the oxidation of fat(s) and thus the concentration and antibody response should reflect the amount of fat in the diet. Objective The purpose of this study was to evaluate the antibody responses to MAA modified proteins following immunization and high fat western diet feeding in rats. Methods Male Sprague Dawley rats were immunized with MAA-modified protein weekly for 5 weeks and then assayed for antibodies to these proteins. Animals were then separated into the following groups: chow sham, chow MAA immunized, high fat sham, and high fat MAA immunized. The high fat animals were fed a Western diet with 2-thiouracil for 12 weeks, bled every 3 weeks, and serum assayed for the presence of circulating MAA antibodies. Results Prior to feeding with high fat diet, rats immunized with MAA-modified protein had a significant increase (P<0.001) in serum antibodies directed against these modified proteins compared to controls (N of 4 per group). Following feeding of high fat diet antibody concentrations increased 6 fold in the high fat MAA immunized group compared to the chow MAA immunized group (P<0.05). Antibodies in the high fat sham and chow sham had only minimal increases in antibodies to these proteins. Conclusions These data demonstrate that following immunization with MAA-modified proteins, circulating antibodies are produced that increase following consumption of a high fat Western diet. It suggests that MAA-modified proteins are produced at low levels following normal diet, producing antibodies which act as a normal clearance method for altered protein. When high fat consumption increases these antibody levels are increased in response to the oxidative stress. Implications Use of these antibodies as a biomarker in the future may help predict the onset or progression of atherosclerosis.


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