scholarly journals Perinatal Iron Deficiency Combined with a High-Fat Diet Causes Obesity and Cardiovascular Dysregulation

Endocrinology ◽  
2012 ◽  
Vol 153 (3) ◽  
pp. 1174-1182 ◽  
Author(s):  
Stephane L. Bourque ◽  
Marina Komolova ◽  
Kristin McCabe ◽  
Michael A. Adams ◽  
Kanji Nakatsu

Consumption of a high-fat Western diet (WD) and the resultant obesity is linked to a number of chronic pathologies, including cardiovascular dysregulation. The purpose of the present study was to determine whether perinatal iron deficiency (PID) added to the consumption of a WD would precipitate an obese phenotype with exacerbated metabolic and cardiovascular outcomes in adult offspring. Female Sprague Dawley rats were fed either a control (225 mg/kg Fe) or an iron-restricted diet (3–10 mg/kg Fe) prior to and throughout gestation. At birth, all dams were fed an iron-replete diet. At weaning, offspring were fed a normal diet or WD for up to 21 wk. Hemodynamics and locomotor activity were assessed by radiotelemetry starting at 15 wk of age. Iron restriction during pregnancy caused severe anemia in dams and offspring, resulting in 15% lower birth weights in the offspring. PID offspring fed the WD had greater caloric intake and exhibited reduced locomotor activity compared with their normal diet-fed littermates; no such effects were observed in normal iron control offspring. Despite having a similar effect on serum lipid profiles, consumption of the WD had a greater impact on body weight in the PID group, and this weight gain was due largely to visceral adipose tissue accumulation. A significant correlation between visceral adipose tissue weight and mean arterial pressure was observed in the PID offspring but not in controls. These observations demonstrate that PID predisposes offspring to an enhanced response to WD characterized by increased fat accumulation and cardiovascular dysregulation.

2020 ◽  
Vol 10 (2) ◽  
pp. 106-117
Author(s):  
Maryam Mostafavian ◽  
◽  
Ahmad Abdi ◽  
Javad Mehrabani ◽  
Alireza Barari ◽  
...  

Objective: Decreased physical activity coupled with increased High‐Fat Diet (HFD) intake prompts obesity. Current research suggests that changing White Adipose Tissue (WAT) to brown promotes energy expenditure to counter obesity. The purpose of this study was to investigate the effects of aerobic Progressive training and Capsaicin (Cap) on Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) and Uncoupling protein-1 (UPC-1) gene expression in rat fed a high-fat diet. Methods: 40 male Wistar rats aged 8-12 weeks, were fed a Normal Diet (ND) (n=8) or HFD (n=32) for 8 weeks. After 8 weeks, rats were divided into 5 groups: ND, HFD, High-Fat Diet-Training (HFDT), High-Fat Diet-Capsaicin (HFDCap), high-fat diet-training-capsaicin (HFDTCap). Training groups have performed a progressive aerobic running program on a motor-driven treadmill for eight weeks. Capsaicin (4 mg/kg/day) were administered orally, by gavage, once a day. PGC-1α and UCP-1 gene expression levels in the VAT were measured by Real-time PCR method. Results: The results of this study showed that PGC-1α and UCP-expression was decreased in HFD group compared to ND group. Also, the expression of PGC-1α and UPC-1 in HFDT, HFDCap and HFDTCap groups was significantly increased compared to HFD. The expression of PGC-1α and UPC-1 in HFDTCap was also significantly increased compared to HFDT and HFDCap groups. Conclusion: Possibly, eight weeks of progressive training combined with capsaicin administration has an effect on the browning of visceral adipose tissue in HFD rats by increasing expression of PGC-1α and UCP-1.


2019 ◽  
Author(s):  
Lisa Y. Beppu ◽  
Xiaoyao Qu ◽  
Giovanni J. Marrero ◽  
Allen N. Fooks ◽  
Adolfo B. Frias ◽  
...  

ABSTRACTCrosstalk between the immune system and adipocytes is critical for maintaining tissue homeostasis and regulating chronic systemic inflammation during diet-induced obesity (DIO). How visceral adipose tissue resident regulatory T cells (aTregs) signal to adipocytes in the visceral adipose tissue (VAT) is not understood. Here we show that Treg-specific ablation of the transcriptional regulator Blimp-1 resulted in increased insulin sensitivity, decreased body weight and increased Ucp-1 in adipocytes in high fat diet (HFD)-fed mice. Mechanistically, we demonstrate that Blimp-1 drives IL-10 production in Tregs, thus suppressing beiging and energy expenditure in adipocytes. Moreover, IL-10 mRNA expression positively correlated with increasing body weight in humans. These findings reveal a surprising relationship between aTregs and adipocytes in promoting insulin resistance during excessive caloric intake, placing Blimp-1-regulated IL-10 expression by aTregs at a critical juncture in the development of obesity and its associated comorbidities in mice and humans.SUMMARYHere we show that ablation of Blimp-1 in adipose tissue resident Tregs (aTregs) leads to decreased IL-10 production, resulting in increased Ucp-1 expression and beiging by adipocytes and protection from diet-induced obesity and insulin resistance.


2021 ◽  
pp. 1-24
Author(s):  
L. Irasema Chávaro-Ortiz ◽  
Brenda D. Tapia-Vargas ◽  
Mariel Rico-Hidalgo ◽  
Ruth Gutiérrez-Aguilar ◽  
María E. Frigolet

Abstract Obesity is defined as increased adiposity, which leads to metabolic disease. The growth of adipose tissue depends on its capacity to expand, through hyperplasia or hypertrophy, in order to buffer energy surplus. Also, during the establishment of obesity, adipose tissue expansion reflects adipose lipid metabolism (lipogenesis and/or lipolysis). It is well known that dietary factors can modify lipid metabolism promoting or preventing the development of metabolic abnormalities that concur with obesity. Trans-palmitoleic acid (TP), a biomarker of dairy consumption, has been associated with reduced adiposity in clinical studies. Thus, we aimed to evaluate the effect of TP over adiposity and lipid metabolism-related genes in a rodent model of diet-induced obesity (DIO). To fulfil this aim, we fed C57BL/6 mice with a Control or a High Fat diet, added with or without TP (3g/kg diet), during 11 weeks. Body weight and food intake were monitored, fat pads were weighted, histology of visceral adipose tissue was analysed, and lipid metabolism-related gene expression was explored by qPCR. Results show that TP consumption prevented weight gain induced by high fat diet, reduced visceral adipose tissue weight, and adipocyte size, while increasing the expression of lipolytic molecules. In conclusion, we show for the first time that TP influences adipose tissue metabolism, specifically lipolysis, resulting in decreased adiposity and reduced adipocyte size in a DIO mice model.


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.


1982 ◽  
Vol 242 (2) ◽  
pp. E93-E96 ◽  
Author(s):  
W. H. Miller ◽  
I. M. Faust

Rats raised in the cold showed an unusual pattern of adipose tissue morphology. Male Sprague-Dawley rats were maintained in a 5 degrees C environment for up to 24 wk and the cellularity of their major adipose depots was determined. Normal age-related increases in adipocyte number were absent in two major fat depots (retroperitoneal and inguinal), whereas there was a supranormal increase in a third (epididymal). This pattern of hyperplasia contrasts sharply with that seen in rats fed highly palatable high-fat or high-carbohydrate diets in which retroperitoneal depots show the most hyperplasia and epididymal pads the least. Such variations of response across depots suggest that the features of adipose tissue responsible for adipocyte proliferation in the various depots may not be homogeneous both in their nature and in their distribution.


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.


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