LIVIVO - The Search Portal for Life Sciences

zur deutschen Oberfläche wechseln
Advanced search

Search results

Result 1 - 10 of total 31

Search options

  1. Article ; Online: The influence of estrogen response element ERα signaling in the control of feeding behaviors in male and female mice.

    Yasrebi, Ali / Regan, Daniel / Roepke, Troy A

    Steroids

    2023  Volume 195, Page(s) 109228

    Abstract: Circulating 17β-estradiol (E2) controls energy homeostasis and feeding behaviors primarily by its nuclear receptor, estrogen receptor (ER) α. As such, it is important to understand the role of ERα signaling in the neuroendocrine control of feeding. Our ... ...

    Abstract Circulating 17β-estradiol (E2) controls energy homeostasis and feeding behaviors primarily by its nuclear receptor, estrogen receptor (ER) α. As such, it is important to understand the role of ERα signaling in the neuroendocrine control of feeding. Our previous data indicated that the loss of ERα signaling through estrogen response elements (ERE) alters food intake in a female mouse model. Hence, we hypothesize that ERE-dependent ERα is necessary for typical feeding behaviors in mice. To test this hypothesis, we examined feeding behaviors on low-fat diet (LFD) and high-fat diet (HFD) in three mouse strains: total ERα knockout (KO), ERα knockin/knockout (KIKO), which lack a functional DNA-binding domain, and their wild type (WT) C57 littermates comparing intact males and females and ovariectomized females with or without E2 replacement. All feeding behaviors were recorded using the Biological Data Acquisition monitoring system (Research Diets). In intact male mice, KO and KIKO consumed less than WT mice on LFD and HFD, while in intact female mice, KIKO consumed less than WT and KO. These differences were primarily driven by shorter meal duration in the KO and KIKO. In ovariectomized females, E2-treated WT and KIKO consumed more LFD than KO driven in part by an increase in meal frequency and a decrease in meal size. On HFD, WT consumed more than KO with E2, again due to effects on meal size and frequency. Collectively, these suggest that both ERE-dependent and -independent ERα signaling are involved in feeding behaviors in female mice depending on the diet consumed.
    MeSH term(s) Mice ; Female ; Male ; Animals ; Estrogen Receptor alpha/genetics ; Receptors, Estrogen ; Mice, Knockout ; Estrogens ; Feeding Behavior ; Response Elements
    Chemical Substances Estrogen Receptor alpha ; Receptors, Estrogen ; Estrogens
    Language English
    Publishing date 2023-03-27
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 80312-1
    ISSN 1878-5867 ; 0039-128X
    ISSN (online) 1878-5867
    ISSN 0039-128X
    DOI 10.1016/j.steroids.2023.109228
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  2. Article ; Online: Intermittent fasting disrupts hippocampal-dependent memory and norepinephrine content in aged male and female mice.

    Wiersielis, Kimberly / Yasrebi, Ali / Degroat, Thomas J / Knox, Nadja / Rojas, Catherine / Feltri, Samantha / Roepke, Troy A

    Physiology & behavior

    2023  Volume 275, Page(s) 114431

    Abstract: Intermittent fasting (IMF) is associated with many health benefits in animals and humans. Yet, little is known if an IMF diet affects mood and cognitive processing. We have previously identified that IMF in diet-induced obese males increases ... ...

    Abstract Intermittent fasting (IMF) is associated with many health benefits in animals and humans. Yet, little is known if an IMF diet affects mood and cognitive processing. We have previously identified that IMF in diet-induced obese males increases norepinephrine and dopamine content in the hypothalamus and increases arcuate neuropeptide Y (NPY) gene expression more than in ad libitum control males. This suggests that IMF may improve cognition through activation of the hindbrain norepinephrine neuronal network and reverse the age-dependent decline in NPY expression. Less is known about the association between anxiety and IMF. Although, in humans, IMF during Ramadan may alleviate anxiety. Here, we address the impact of IMF on anxiety-like behavior using the open field test, hippocampal-dependent memory using the Y-maze and spatial object recognition, and hippocampal-independent memory using novel object recognition in middle-aged male and female (12 mo) and aged male and female (18 mo) mice. Using ELISA, we determined norepinephrine (NE) content in the dorsal hippocampus (DH) and prefrontal cortex (PFC). We also investigated gene expression in the arcuate nucleus (ARC), the lateral hypothalamus (LH), and the locus coeruleus (LC). In IMF-treated females at both ages, we observed an improvement in spatial navigation although an impairment in spatial object orientation. IMF-treated females (12 mo) had a reduction and IMF-treated males (12 mo) displayed an improvement in novel object recognition memory. IMF-treated females (18 mo) exhibited anxiolytic-like behavior and increased locomotion. In the DH, IMF-treated males (12 mo) had a greater amount of NE content and IMF-treated males (18 mo) had a reduction. In the ARC, IMF-treated males (12 mo) exhibited an increase in Agrp and Npy and a decrease in Adr1a. In the ARC, IMF-treated males (18 mo) exhibited an increase in Npy and a decrease in Adr1a; females had a trending decrease in Cart. In the LH at 12 months, IMF-treated males had a decrease in Npy5r, Adr1a, and Adr1b; both males and females had a reduction in Npy1r. In the LH, IMF-treated females (18 mo) had a decrease in Hcrt. In the LC at both ages, mice largely exhibited sex effects. Our findings indicate that IMF produces alterations in mood, cognition, DH NE content, and ARC, LH, and LC gene expression depending on sex and age.
    MeSH term(s) Humans ; Mice ; Male ; Female ; Animals ; Middle Aged ; Aged ; Norepinephrine/metabolism ; Intermittent Fasting ; Neuropeptide Y/metabolism ; Hypothalamus/metabolism ; Hippocampus/metabolism
    Chemical Substances Norepinephrine (X4W3ENH1CV) ; Neuropeptide Y
    Language English
    Publishing date 2023-12-10
    Publishing country United States
    Document type Journal Article
    ZDB-ID 3907-x
    ISSN 1873-507X ; 0031-9384
    ISSN (online) 1873-507X
    ISSN 0031-9384
    DOI 10.1016/j.physbeh.2023.114431
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  3. Article ; Online: The influence of estrogen receptor α signaling independent of the estrogen response element on avoidance behavior, social interactions, and palatable ingestive behavior in female mice.

    Wiersielis, Kimberly / Yasrebi, Ali / Ramirez, Patricia / Verpeut, Jessica / Regan, Daniel / Roepke, Troy A

    Hormones and behavior

    2021  Volume 136, Page(s) 105084

    Abstract: Women are vulnerable to developing mental disorders that are associated with circulating estrogens. Estrogens, especially 17β-estradiol (E2), have a wide array of effects on the brain, affecting many behavioral endpoints associated with mental illness. ... ...

    Abstract Women are vulnerable to developing mental disorders that are associated with circulating estrogens. Estrogens, especially 17β-estradiol (E2), have a wide array of effects on the brain, affecting many behavioral endpoints associated with mental illness. By using a total estrogen receptor (ER) α knockout (KO), an ERα knock in/knock out (KIKO) that lacks a functional DNA-binding domain, and wild type (WT) controls treated with either oil or E2, we evaluated ERα signaling, dependent and independent of the estrogen response element (ERE), on avoidance behavior, social interactions and memory, and palatable ingestive behavior using the open field test, the elevated plus maze, the light dark box, the 3-chamber test, and palatable feeding. We found that ERα does not mediate control of anxiety-like behaviors but rather yielded differences in locomotor activity. In evaluating social preference and social recognition memory, we observed that E2 may modulate these measures in KIKO females but not KO females, suggesting that ERE-independent signaling is likely involved in sociability. Lastly, observations of palatable (high-fat) food intake suggested an increase in palatable eating behavior in oil-treated KIKO females. Oil-treated KO females had a longer latency to food intake, indicative of an anhedonic phenotype compared to oil-treated WT and KIKO females. We have observed that social-related behaviors are potentially influenced by ERE-independent ERα signaling and hedonic food intake requires signaling of ERα.
    MeSH term(s) Animals ; Avoidance Learning ; Behavior, Animal ; Estradiol/pharmacology ; Estradiol/physiology ; Estrogen Receptor alpha/genetics ; Estrogens/pharmacology ; Feeding Behavior ; Female ; Mice ; Mice, Knockout ; Response Elements ; Social Interaction
    Chemical Substances Estrogen Receptor alpha ; Estrogens ; Estradiol (4TI98Z838E)
    Language English
    Publishing date 2021-10-30
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 214409-8
    ISSN 1095-6867 ; 0018-506X
    ISSN (online) 1095-6867
    ISSN 0018-506X
    DOI 10.1016/j.yhbeh.2021.105084
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  4. Article: Implications of estrogen receptor alpha (ERa) with the intersection of organophosphate flame retardants and diet-induced obesity in adult mice.

    Vail, Gwyndolin M / Walley, Sabrina N / Yasrebi, Ali / Maeng, Angela / Degroat, Thomas J / Conde, Kristie M / Roepke, Troy A

    Journal of toxicology and environmental health. Part A

    2022  Volume 85, Issue 10, Page(s) 397–413

    Abstract: Previously, organophosphate flame retardants (OPFRs) were found to produce intersecting disruptions of energy homeostasis using an adult mouse model of diet-induced obesity. Using the same mixture consisting of 1 mg/kg/day of each triphenyl phosphate, ... ...

    Abstract Previously, organophosphate flame retardants (OPFRs) were found to produce intersecting disruptions of energy homeostasis using an adult mouse model of diet-induced obesity. Using the same mixture consisting of 1 mg/kg/day of each triphenyl phosphate, tricresyl phosphate, and tris(1,3-dichloro-2-propyl)phosphate, the current study aimed to identify the role of estrogen receptor alpha (ERα) in OPFR-induced disruption, utilizing ERα knockout (ERαKO) mice fed either a low-fat diet (LFD) or high-fat diet (HFD). Body weight and composition, food intake patterns, glucose and insulin tolerance, circulating peptide hormones, and expression of hypothalamic genes associated with energy homeostasis were measured. When fed HFD, no marked direct effects of OPFR were observed in mice lacking ERα, suggesting a role for ERα in generating previously reported wildtype (WT) findings. Male ERαKO mice fed LFD experienced decreased feeding efficiency and altered insulin tolerance, whereas their female counterparts displayed less fat mass and circulating ghrelin when exposed to OPFRs. These effects were not noted in the previous WT study, indicating that loss of ERα may sensitize animals fed LFD to alternate pathways of endocrine disruption by OFPRs. Collectively, these data demonstrate both direct and indirect actions of OPFRs on ERα-mediated pathways governing energy homeostasis and support a growing body of evidence urging concern for risk of human exposure.
    MeSH term(s) Animals ; Diet, High-Fat/adverse effects ; Estrogen Receptor alpha/genetics ; Estrogen Receptor alpha/metabolism ; Female ; Flame Retardants/toxicity ; Insulin ; Male ; Mice ; Obesity/chemically induced ; Obesity/metabolism ; Organophosphates
    Chemical Substances Estrogen Receptor alpha ; Flame Retardants ; Insulin ; Organophosphates
    Language English
    Publishing date 2022-01-19
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1413345-3
    ISSN 1528-7394 ; 0098-4108 ; 1087-2620
    ISSN 1528-7394 ; 0098-4108 ; 1087-2620
    DOI 10.1080/15287394.2022.2026849
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  5. Article: Implications of peroxisome proliferator-activated receptor gamma (PPARY) with the intersection of organophosphate flame retardants and diet-induced obesity in adult mice.

    Vail, Gwyndolin M / Walley, Sabrina N / Yasrebi, Ali / Maeng, Angela / Degroat, Thomas J / Conde, Kristie M / Roepke, Troy A

    Journal of toxicology and environmental health. Part A

    2022  Volume 85, Issue 9, Page(s) 381–396

    Abstract: Previously, organophosphate flame retardants (OPFRs) were demonstrated to dysregulate homeostatic parameters of energy regulation within an adult mouse model of diet-induced obesity. Using the same OPFR mixture consisting of 1 mg/kg/day of each triphenyl ...

    Abstract Previously, organophosphate flame retardants (OPFRs) were demonstrated to dysregulate homeostatic parameters of energy regulation within an adult mouse model of diet-induced obesity. Using the same OPFR mixture consisting of 1 mg/kg/day of each triphenyl phosphate, tricresyl phosphate, and tris(1,3-dichloro-2-propyl)phosphate, the current study examined the role of peroxisome proliferator-activated receptor gamma (PPARγ) in OPFR-induced disruption by utilizing mice with brain-specific deletion of PPARγ (PPARγKO) fed either a low-fat diet (LFD) or high-fat diet (HFD). Body weight and composition, feeding behavior, glucose and insulin tolerance, circulating peptide hormones, and expression of hypothalamic genes associated with energy homeostasis were recorded. When fed HFD, the effects of OPFR on body weight and feeding behavior observed in the previous wild-type (WT) study were absent in mice lacking neuronal PPARγ. This posits PPARγ as an important target for eliciting OPFR disruption in a diet-induced obesity model. Interestingly, female PPARγKO mice, but not males, experienced many novel OPFR effects not noted in WT mice, including decreased fat mass, altered feeding behavior and efficiency, improved insulin sensitivity, elevated plasma ghrelin and hypothalamic expression of its receptor. Taken together, these data suggest both direct roles for PPARγ in OPFR disruption of obese mice and indirect sensitization of pathways alternative to PPARγ when neuronal expression is deleted.
    MeSH term(s) Animals ; Diet, High-Fat/adverse effects ; Female ; Flame Retardants ; Mice ; Obesity/chemically induced ; Obesity/metabolism ; Organophosphates ; PPAR gamma/genetics
    Chemical Substances Flame Retardants ; Organophosphates ; PPAR gamma
    Language English
    Publishing date 2022-01-09
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1413345-3
    ISSN 1528-7394 ; 0098-4108 ; 1087-2620
    ISSN 1528-7394 ; 0098-4108 ; 1087-2620
    DOI 10.1080/15287394.2021.2023716
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  6. Article: The interactions of diet-induced obesity and organophosphate flame retardant exposure on energy homeostasis in adult male and female mice.

    Vail, Gwyndolin M / Walley, Sabrina N / Yasrebi, Ali / Maeng, Angela / Conde, Kristie M / Roepke, Troy A

    Journal of toxicology and environmental health. Part A

    2020  Volume 83, Issue 11-12, Page(s) 438–455

    Abstract: Previously, sex-dependent alterations in energy homeostasis were reported in adult mice fed a standard chow attributed to exposure to a mixture of organophosphate flame retardants (OPFRs) via estrogen receptors (ERα). In this study, adult male and female ...

    Abstract Previously, sex-dependent alterations in energy homeostasis were reported in adult mice fed a standard chow attributed to exposure to a mixture of organophosphate flame retardants (OPFRs) via estrogen receptors (ERα). In this study, adult male and female mice (C57BL/6J; Taconic) were treated with the same mixture of OPFRs (1 mg/kg each of tricresyl phosphate (TCP), triphenyl phosphate (TPP), and tris(1-3-dichloro-2propyl)phosphate (TDCPP)) for 7 weeks on a low-fat diet (LFD, 10% kcal fat) or a high fat (HFD, 45% kcal fat) in a diet-induced obesity model. Consistent with our previous observations, OPFRs altered weight gain in males, differentially with diet, while females remained unaffected. OPFR treatment also revealed sex-dependent perturbations in metabolic activity. During the night (approximately 0100-0400 hr), males exhibited elevated activity and oxygen consumption, while in females these parameters were decreased, irrespective of diet. OPFR disrupted feeding behavior and abolished diurnal water intake patterns in females while increasing nighttime fluid consumption in males. Despite no marked effect of OPFRs on glucose or insulin tolerance, OPFR treatment altered circulating insulin and leptin in females and ghrelin in males. Data indicate that adult OPFR exposure might influence, and perhaps exacerbate, the effects of diet-induced obesity in adult mice by altering activity, ingestive behavior, and metabolism.
    MeSH term(s) Animals ; Dietary Exposure/adverse effects ; Energy Metabolism/drug effects ; Feeding Behavior/drug effects ; Female ; Flame Retardants/toxicity ; Homeostasis/drug effects ; Male ; Mice ; Mice, Inbred C57BL ; Motor Activity/drug effects ; Obesity/etiology ; Obesity/metabolism ; Organophosphates/toxicity ; Peptide Hormones/blood ; Sex Factors ; Weight Gain/drug effects
    Chemical Substances Flame Retardants ; Organophosphates ; Peptide Hormones
    Language English
    Publishing date 2020-06-16
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1413345-3
    ISSN 1528-7394 ; 0098-4108 ; 1087-2620
    ISSN 1528-7394 ; 0098-4108 ; 1087-2620
    DOI 10.1080/15287394.2020.1777235
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  7. Article ; Online: Linoleic acid causes greater weight gain than saturated fat without hypothalamic inflammation in the male mouse.

    Mamounis, Kyle J / Yasrebi, Ali / Roepke, Troy A

    The Journal of nutritional biochemistry

    2017  Volume 40, Page(s) 122–131

    Abstract: A significant change in the Western diet, concurrent with the obesity epidemic, was a substitution of saturated fatty acids with polyunsaturated, specifically linoleic acid (LA). Despite increasing investigation on type as well as amount of fat, it is ... ...

    Abstract A significant change in the Western diet, concurrent with the obesity epidemic, was a substitution of saturated fatty acids with polyunsaturated, specifically linoleic acid (LA). Despite increasing investigation on type as well as amount of fat, it is unclear which fatty acids are most obesogenic. The objective of this study was to determine the obesogenic potency of LA vs. saturated fatty acids and the involvement of hypothalamic inflammation. Forty-eight mice were divided into four groups: low-fat or three high-fat diets (HFDs, 45% kcals from fat) with LA comprising 1%, 15% and 22.5% of kilocalories, the balance being saturated fatty acids. Over 12 weeks, bodyweight, body composition, food intake, calorimetry, and glycemia assays were performed. Arcuate nucleus and blood were collected for mRNA and protein analysis. All HFD-fed mice were heavier and less glucose tolerant than control. The diet with 22.5% LA caused greater bodyweight gain, decreased activity, and insulin resistance compared to control and 1% LA. All HFDs elevated leptin and decreased ghrelin in plasma. Neuropeptides gene expression was higher in 22.5% HFD. The inflammatory gene Ikk was suppressed in 1% and 22.5% LA. No consistent pattern of inflammatory gene expression was observed, with suppression and augmentation of genes by one or all of the HFDs relative to control. These data indicate that, in male mice, LA induces obesity and insulin resistance and reduces activity more than saturated fat, supporting the hypothesis that increased LA intake may be a contributor to the obesity epidemic.
    MeSH term(s) Animals ; Carbon Dioxide/metabolism ; Chemokine CX3CL1/metabolism ; Diet, Fat-Restricted ; Encephalitis/chemically induced ; Encephalitis/etiology ; Encephalitis/pathology ; Fatty Acids/adverse effects ; Ghrelin/blood ; Glucose/metabolism ; Hypothalamus/pathology ; Leptin/blood ; Linoleic Acid/adverse effects ; Male ; Mice, Inbred C57BL ; Weight Gain/drug effects
    Chemical Substances Chemokine CX3CL1 ; Cx3cl1 protein, mouse ; Fatty Acids ; Ghrelin ; Leptin ; Carbon Dioxide (142M471B3J) ; Linoleic Acid (9KJL21T0QJ) ; Glucose (IY9XDZ35W2)
    Language English
    Publishing date 2017
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 1014929-6
    ISSN 1873-4847 ; 0955-2863
    ISSN (online) 1873-4847
    ISSN 0955-2863
    DOI 10.1016/j.jnutbio.2016.10.016
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  8. Article: Linoleic acid causes greater weight gain than saturated fat without hypothalamic inflammation in the male mouse

    Mamounis, Kyle J / Roepke, Troy A / Yasrebi, Ali

    Journal of nutritional biochemistry. 2017 Feb., v. 40

    2017  

    Abstract: A significant change in the Western diet, concurrent with the obesity epidemic, was a substitution of saturated fatty acids with polyunsaturated, specifically linoleic acid (LA). Despite increasing investigation on type as well as amount of fat, it is ... ...

    Abstract A significant change in the Western diet, concurrent with the obesity epidemic, was a substitution of saturated fatty acids with polyunsaturated, specifically linoleic acid (LA). Despite increasing investigation on type as well as amount of fat, it is unclear which fatty acids are most obesogenic. The objective of this study was to determine the obesogenic potency of LA vs. saturated fatty acids and the involvement of hypothalamic inflammation. Forty-eight mice were divided into four groups: low-fat or three high-fat diets (HFDs, 45% kcals from fat) with LA comprising 1%, 15% and 22.5% of kilocalories, the balance being saturated fatty acids. Over 12 weeks, bodyweight, body composition, food intake, calorimetry, and glycemia assays were performed. Arcuate nucleus and blood were collected for mRNA and protein analysis. All HFD-fed mice were heavier and less glucose tolerant than control. The diet with 22.5% LA caused greater bodyweight gain, decreased activity, and insulin resistance compared to control and 1% LA. All HFDs elevated leptin and decreased ghrelin in plasma. Neuropeptides gene expression was higher in 22.5% HFD. The inflammatory gene Ikk was suppressed in 1% and 22.5% LA. No consistent pattern of inflammatory gene expression was observed, with suppression and augmentation of genes by one or all of the HFDs relative to control. These data indicate that, in male mice, LA induces obesity and insulin resistance and reduces activity more than saturated fat, supporting the hypothesis that increased LA intake may be a contributor to the obesity epidemic.
    Keywords blood ; blood glucose ; calorimetry ; food intake ; gene expression ; genes ; ghrelin ; glucose ; high fat diet ; inflammation ; insulin resistance ; leptin ; linoleic acid ; males ; messenger RNA ; mice ; neuropeptides ; obesity ; polyunsaturated fatty acids ; saturated fats ; saturated fatty acids ; weight gain ; Western diets
    Language English
    Dates of publication 2017-02
    Size p. 122-131.
    Publishing place Elsevier Inc.
    Document type Article
    ZDB-ID 1014929-6
    ISSN 1873-4847 ; 0955-2863
    ISSN (online) 1873-4847
    ISSN 0955-2863
    DOI 10.1016/j.jnutbio.2016.10.016
    Database NAL-Catalogue (AGRICOLA)

    More links

    Kategorien

  9. Article ; Online: The effects of dietary fatty acids in the physiological outcomes of maternal high-fat diet on offspring energy homeostasis in mice.

    Mamounis, Kyle J / Shvedov, Naomi R / Margolies, Nicholas / Yasrebi, Ali / Roepke, Troy A

    Journal of developmental origins of health and disease

    2019  Volume 11, Issue 3, Page(s) 273–284

    Abstract: The early-life origins of disease hypothesis has been applied to obesity research and modeled through overnutrition, usually with a high-fat diet (HFD). Since the obesity epidemic coincided with societal change in dietary fat consumption, rather than ... ...

    Abstract The early-life origins of disease hypothesis has been applied to obesity research and modeled through overnutrition, usually with a high-fat diet (HFD). Since the obesity epidemic coincided with societal change in dietary fat consumption, rather than amount, manipulation of fatty acid (FA) profile is an under-investigated area of study. Additionally, the binding of FAs to nuclear receptors may have persistent intergenerational, extranutritive endocrinological effects that interact with the actions of reproductive steroids causing sex-dependent effects. To determine the role of FA type in the effects underlying maternal HFD, we fed wild-type C57BL6/J mating pairs, from preconception through lactation, a HFD with high saturated fat levels from coconut oil or high linoleic acid (LA) levels from vegetable oil. Male and female offspring body weight and food intake were measured weekly for 25 weeks. Assays for glucose metabolism, body composition, and calorimetry were performed at 25 weeks. Plasma metabolic peptides and liver mRNA were measured terminally. Obesity was primarily affected by adult rather than maternal diet in males, yet in females, maternal HFD potentiated the effects of adult HFD. Maternal HFD high in LA impaired glucose disposal in males weaned onto HFD and insulin sensitivity of females. Plasma leptin correlated with adiposity, but insulin and insulin receptor expression in the liver were altered by maternal LA in males. Our results suggest that maternal FA profile is most influential on offspring glucose metabolism and that adult diet is more important than maternal diet for obesity and other parameters of metabolic syndrome.
    MeSH term(s) Adiposity/physiology ; Animals ; Animals, Suckling/metabolism ; Body Weight/physiology ; Diet, High-Fat/adverse effects ; Dietary Fats/adverse effects ; Disease Models, Animal ; Energy Metabolism/physiology ; Fatty Acids/adverse effects ; Female ; Humans ; Infant ; Infant Nutritional Physiological Phenomena ; Insulin/metabolism ; Insulin Resistance/physiology ; Lactation ; Male ; Maternal Nutritional Physiological Phenomena ; Mice ; Obesity/epidemiology ; Obesity/metabolism ; Pregnancy ; Sex Factors ; Weaning
    Chemical Substances Dietary Fats ; Fatty Acids ; Insulin
    Language English
    Publishing date 2019-09-26
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2554780-X
    ISSN 2040-1752 ; 2040-1744
    ISSN (online) 2040-1752
    ISSN 2040-1744
    DOI 10.1017/S2040174419000540
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

  10. Article ; Online: The loss of ERE-dependent ERα signaling potentiates the effects of maternal high-fat diet on energy homeostasis in female offspring fed an obesogenic diet.

    Roepke, Troy A / Yasrebi, Ali / Villalobos, Alejandra / Krumm, Elizabeth A / Yang, Jennifer A / Mamounis, Kyle J

    Journal of developmental origins of health and disease

    2019  Volume 11, Issue 3, Page(s) 285–296

    Abstract: Maternal high-fat diet (HFD) alters hypothalamic programming and disrupts offspring energy homeostasis in rodents. We previously reported that the loss of ERα signaling partially blocks the effects of maternal HFD in female offspring fed a standard chow ... ...

    Abstract Maternal high-fat diet (HFD) alters hypothalamic programming and disrupts offspring energy homeostasis in rodents. We previously reported that the loss of ERα signaling partially blocks the effects of maternal HFD in female offspring fed a standard chow diet. In a companion study, we determined if the effects of maternal HFD were magnified by an adult obesogenic diet in our transgenic mouse models. Heterozygous ERα knockout (wild-type (WT)/KO) dams were fed a control breeder chow diet (25% fat) or a semipurified HFD (45% fat) 4 weeks prior to mating with heterozygous males (WT/KO or WT/ knockin) to produce WT, ERα KO, or ERα knockin/knockout (KIKO) (no estrogen response element (ERE) binding) female offspring, which were fed HFD for 20 weeks. Maternal HFD potentiated the effects of adult HFD on KIKO and KO body weight due to increased adiposity and decreased activity. Maternal HFD also produced KIKO females that exhibit KO-like insulin intolerance and impaired glucose homeostasis. Maternal HFD increased plasma interleukin 6 and monocyte chemoattractant protein 1 levels and G6pc and Pepck liver expression only in WT mice. Insulin and tumor necrosis factor α levels were higher in KO offspring from HFD-fed dams. Arcuate and liver expression of Esr1 was altered in KIKO and WT, respectively. These data suggest that loss of ERE-dependent ERα signaling, and not total ERα signaling, sensitizes females to the deleterious influence of maternal HFD on offspring energy and glucose potentially through the control of peripheral inflammation and hypothalamic and liver gene expression. Future studies will interrogate the tissue-specific mechanisms of maternal HFD programming through ERα signaling.
    MeSH term(s) Animals ; Diet, High-Fat/adverse effects ; Disease Models, Animal ; Energy Metabolism/genetics ; Estrogen Receptor alpha/genetics ; Estrogen Receptor alpha/metabolism ; Female ; Gene Expression Regulation, Developmental ; Gene Knock-In Techniques ; Genetic Predisposition to Disease ; Humans ; Infant ; Infant Nutritional Physiological Phenomena ; Male ; Maternal Nutritional Physiological Phenomena ; Mice ; Mice, Knockout ; Obesity/etiology ; Response Elements ; Sex Factors ; Signal Transduction/genetics
    Chemical Substances Esr1 protein, mouse ; Estrogen Receptor alpha
    Language English
    Publishing date 2019-09-23
    Publishing country England
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, U.S. Gov't, Non-P.H.S.
    ZDB-ID 2554780-X
    ISSN 2040-1752 ; 2040-1744
    ISSN (online) 2040-1752
    ISSN 2040-1744
    DOI 10.1017/S2040174419000515
    Database MEDical Literature Analysis and Retrieval System OnLINE

    More links

    Kategorien

To top