Exposure to maternal hyperglycemia and high-fat diet consumption after weaning in rats: repercussions on periovarian adipose tissue

2021 ◽  
pp. 1-8
Author(s):  
Carolina M. Saullo ◽  
Yuri K. Sinzato ◽  
Verônyca G. Paula ◽  
Franciane Q. Gallego ◽  
José E. Corrente ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Adult Life ◽  
Maternal Diabetes ◽  
Female Offspring ◽  
Standard Diet ◽  
High Fat ◽  
Intrauterine Environment ◽  
Tissue Samples ◽  
Maternal Hyperglycemia

Abstract Clinical and epidemiological studies show that maternal hyperglycemia can change the programming of offspring leading to transgenerational effects. These changes may be related to environmental factors, such as high-fat diet (HFD) consumption, and contribute to the comorbidity onset at the adulthood of the offspring. The objective of this study was to evaluate the hyperglycemic intrauterine environment, associated or not with an HFD administered from weaning to adult life on the periovarian adipose tissue of rat offspring Maternal diabetes was chemically induced by Streptozotocin. Female offsprings were randomly distributed into four experimental groups (n = 5 animals/group): Female offspring from control or diabetic mothers and fed an HFD or standard diet. HFD was prepared with lard enrichment and given from weaning to adulthood. On day 120 of life, the rats were anesthetized and sacrificed to obtain adipose tissue samples. Then, the hyperglycemic intrauterine environment and HFD fed after weaning caused a higher body weight, total fat, and periovarian fat in adult offspring, which could compromise the future reproductive function of these females. These rats showed higher adiposity index and adipocyte area, contributing to hypertrophied adipose tissue. Therefore, maternal diabetes itself causes intergenerational changes and, in association with the HFD consumption after weaning, exacerbated the changes in the adipose tissue of adult female offspring.

scholarly journals Differential organ-specific inflammatory response to progranulin in high-fat diet-fed mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Maki Murakoshi ◽  
Tomohito Gohda ◽  
Eri Adachi ◽  
Saki Ichikawa ◽  
Shinji Hagiwara ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Kidney Injury ◽  
Proximal Tubules ◽  
Tubular Damage ◽  
Standard Diet ◽  
Mrna Levels ◽  
High Fat ◽  
Organ Specific

AbstractProgranulin (PGRN) has been reported to bind tumor necrosis factor (TNF) receptor and to inhibit TNFα signaling. We evaluated the effect of augmentation of TNFα signaling by PGRN deficiency on the progression of kidney injury. Eight-week-old PGRN knockout (KO) and wild-type (WT) mice were fed a standard diet or high-fat diet (HFD) for 12 weeks. Albuminuria, markers of tubular damage, and renal mRNA levels of inflammatory cytokines were higher in HFD-fed KO (KO-HFD) mice than in HFD-fed WT (WT-HFD) mice. Body weight, vacuolization in proximal tubules, and systemic and adipose tissue inflammatory markers were lower in the KO-HFD mice than in the WT-HFD mice. The renal megalin expression was lower in the KO mice than in the WT mice regardless of the diet type. The megalin expression was also reduced in mouse proximal tubule epithelial cells stimulated with TNFα and in those with PGRN knockdown by small interfering RNA in vitro. PGRN deficiency was associated with both exacerbated renal inflammation and decreased systemic inflammation, including that in the adipose tissue of mice with HFD-induced obesity. Improved tubular vacuolization in the KO-HFD mice might partially be explained by the decreased expression of megalin in proximal tubules.

Effects of Maternal Hyperglycemia Associated with Snack Intake on Male and Female Offspring High-Fat Diet Preference on Infancy

Metabolism ◽  
2021 ◽  
Vol 116 ◽  
pp. 154635
Author(s):  
Gustavo Venâncio da Silva ◽  
Marina Galleazzo Martins ◽  
Giovana Pereira de Oliveira ◽  
Alessandra Gonçalves Cruz ◽  
Larissa Pereira Rodrigues ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Female Offspring ◽  
High Fat ◽  
Male And Female ◽  
Maternal Hyperglycemia ◽  
Diet Preference

scholarly journals Chia Seed (Salvia hispanica L.) Digested Total Protein Prevented Adipose Tissue Inflammation and Reduce Obesity Complications in Mice Fed a High-Fat Diet

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 436-436
Author(s):  
Hercia Martino ◽  
Mariana Grancieri ◽  
Renata Toledo ◽  
Thaisa Veridiano ◽  
Cintia Tomaz Sant'Ana ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Waist Circumference ◽  
Total Cholesterol ◽  
High Fat Diet ◽  
Negative Control ◽  
Standard Diet ◽  
Adipose Tissue Inflammation ◽  
High Fat ◽  
Tissue Inflammation ◽  
Chia Seed

Abstract Objectives To evaluate the effects of digested total proteins (DTP) from chia seed to prevent adipogenesis and adipose tissue inflammation in mice fed a high-fat diet. Methods C57Bl/6 black mice (n = 44; 8 weeks old) where divided in 4 groups (n = 12 each): negative control (NC; standard diet AIN-93M); positive control (PC; high fat diet- HFD- 60% of lipids); normal diet + DTP (NH; standard diet + 400 mg/kg of body/day of DTP); high-fat diet plus DTP (HFH; HFD + 400 mg/kg of body/day of DTP). After 9 weeks of treatment, the animals were euthanized and the blood and the adipose tissue (total) were collected. Plasma was used to analyze total cholesterol, high-density (HDL) and low-density (LDL) lipoprotein cholesterol, triacylglycerides (TGL), aspartate (AST) and alanine (ALT) aminotransferase levels by colorimetry. Waist circumference was measured by metric tape in the middle portion between the anus and mouth and the quantity of p-p65-NF-κB and PPAR-Y ELISA test. Histomorphometric analysis was determined in adipose tissue staining with hematoxylin/eosin to determined adipocytes area and foci of inflammation by the average of 1000 cells/group. Data were analyzed by ANOVA and post-hoc of Newman-Kews (P < 0.05). The study protocol was approved by the Ethics Committee of the Federal University of Viçosa (Protocol 01/2019). Results DTP from chia seed reduced the plasmatic levels of total cholesterol (−17.5%), LDL (−42.8%), TGL (−12.3%), and waist circumference (−5.5%) in obesity mice DTP-treated (P < 0.05). The treatment with DTP reduced the adipocytes area in HFH group by −15.1% and the foci of inflammation in −78.1% in comparison with PC (P < 0.05). The levels of p-p65-NF-κB in adipose tissue were reduced by DTP in mice fed a HFD in −41.1% (P < 0.05). However, PPAR-γ levels, body fat (%), Lee index, and HDL levels were not changed by DTP (P > 0.05). The levels of AST and ALT were not affected by HFD or DTP (P > 0.05). Conclusions DTP from chia seed had an anti-inflammatory and even an anti-adipogenic effect. These results show the effectiveness of digested proteins from chia seed against obesity and its associated inflammation. Funding Sources CNPq and CAPES (Brazil), and ACES (USA).

Abstract 023: Inducible Deletion of Adipocyte Prorenin Receptor Reverses Obesity Related Hypertension

Hypertension ◽  
2017 ◽  
Vol 70 (suppl_1) ◽  
Author(s):  
Eva Gatineau ◽  
Dianne Cohn ◽  
Ming Gong ◽  
Frédérique Yiannikouris
Keyword(s):  
Blood Pressure ◽  
Adipose Tissue ◽  
Lipid Metabolism ◽  
Fat Mass ◽  
High Fat Diet ◽  
Standard Diet ◽  
Mrna Levels ◽  
High Fat ◽  
Elevated Systolic Blood Pressure ◽  
Prorenin Receptor

Obesity contributes to approximatively 2.5 million deaths every year and is associated with life threatening conditions including hypertension. Recently, we found that constitutive deletion of adipocyte (pro)renin-receptor (PRR) prevented high-fat diet-induced obesity through a drastic decrease in fat mass. However, adipocyte PRR deficient mice were characterized by a fatty liver and by an elevated systolic blood pressure (SBP), classic features of models of lipodystrophy. The purpose of this study was to investigate whether the temporally-controlled deletion of adipocyte PRR in obese mice reverses obesity related hypertension. After 18 weeks of high fat diet, inducible adipocyte-PRR deficient ( PRR ERT ) and control ( PRR fl/Y ) male mice (n=7-11 mice/ group) were injected intraperitoneally with tamoxifen (TMX) for 5 consecutive days. Body weight, body composition and blood pressure, measured by radiotelemetry in a subgroup of mice (n=2-4 mice/ group), were recorded before and after TMX injection. The inducible deletion of adipocyte PRR in PRR ERT mice decreased significantly body weights ( PRR fl/fl , 46.6 ± 1.3 g; PRR ERT , 42.1 ± 1.4 g, P<0.05) and fat mass ( PRR fl/fl , 15.8 ± 1.0 g; PRR ERT , 8.1 ± 0.7 g, P<0.05) compared to control mice. PPARγ, FABP4 and FAS mRNA levels were significantly decreased by 68% (6.8 out 10), 80% (8 out 10) and 68% (6.8 out 10) respectively in white adipose tissues of PRR ERT mice suggesting that PRR positively regulated adipogenesis and lipid metabolism in adipose tissue. In addition, the inducible deletion of adipocyte PRR in PRR ERT mice decreased significantly SBP compared to control mice ( PRR fl/fl , -4.3 ± 3.2 g; PRR ERT , -10.2 ± 2.4 g, P<0.05). Interestingly, adipocyte angiotensinogen mRNA abundance was significantly decreased in adipose tissue of PRR ERT mice fed a standard diet suggesting that the decrease in blood pressure might be mediated by a local renin angiotensin system (RAS). The measurement of local (liver, kidney, adipose tissue and brain) and systemic RAS in HF-fed mice is under investigation. Taken together, our results highlight a new signaling pathway in which PRR regulates adipogenesis, lipid metabolism and blood pressure. PRR could represent a new potential therapeutic target for obesity and hypertension.

scholarly journals PTPIP51: A New Interaction Partner of the Insulin Receptor and PKA in Adipose Tissue

2013 ◽  
Vol 2013 ◽  
pp. 1-7 ◽  
Author(s):  
M. A. Bobrich ◽  
S. A. Schwabe ◽  
A. Brobeil ◽  
M. Viard ◽  
M. Kamm ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Insulin Receptor ◽  
Endurance Training ◽  
High Fat Diet ◽  
Insulin Signalling ◽  
Tyrosine Phosphatase ◽  
Proximity Ligation Assay ◽  
Standard Diet ◽  
High Fat ◽  
Insulin Signalling Pathway

Aims. Our previous experiments revealed an association of PTPIP51 (protein tyrosine phosphatase interacting protein 51) with the insulin signalling pathway through PTP1B and 14-3-3beta. We aimed to clarify the role of PTPIP51 in adipocyte metabolism.Methods. Four groups of ten C57Bl/6 mice each were used. Two groups were fed a standard diet; two groups were fed a high-fat diet. Two groups (one high-fat diet and one standard diet) were submitted to endurance training, while the remaining two groups served as untrained control groups. After ten weeks, we measured glucose tolerance of the mice. Adipose tissue samples were analyzed by immunofluorescence and Duolink proximity ligation assay to quantify interactions of PTPIP51 with either insulin receptor (IR) or PKA.Results. PTPIP51 and the IR and PTPIP51 and PKA, respectively, were colocalized in all groups. Standard diet animals that were submitted to endurance training showed low PTPIP51-IR and PTPIP51-PKA interactions. The interaction levels of both the IR and PKA differed between the feeding and training groups.Conclusion. PTPIP51 might serve as a linking protein in adipocyte metabolism by connecting the IR-triggered lipogenesis with the PKA-dependent lipolysis. PTPIP51 interacts with both proteins, therefore being a potential gateway for the cooperation of both pathways.

scholarly journals 3,5-Diiodo-L-Thyronine (T2) Administration Affects Visceral Adipose Tissue Inflammatory State in Rats Receiving Long-Lasting High-Fat Diet

2021 ◽  
Vol 12 ◽  
Author(s):  
Giuseppe Petito ◽  
Federica Cioffi ◽  
Elena Silvestri ◽  
Rita De Matteis ◽  
Davide Lattanzi ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Adverse Effects ◽  
High Fat Diet ◽  
Expression Profiles ◽  
Metabolic Effects ◽  
Daily Injection ◽  
Standard Diet ◽  
High Fat ◽  
Inflammatory Status ◽  
Inflammatory State

3,5-diiodo-thyronine (T2), an endogenous metabolite of thyroid hormones, exerts beneficial metabolic effects. When administered to overweight rats receiving a high fat diet (HFD), it significantly reduces body fat accumulation, which is a risk factor for the development of an inflammatory state and of related metabolic diseases. In the present study, we focused our attention on T2 actions aimed at improving the adverse effects of long-lasting HFD such as the adipocyte inflammatory response. For this purpose, three groups of rats were used throughout: i) receiving a standard diet for 14 weeks; ii) receiving a HFD for 14 weeks, and iii) receiving a HFD for 14 weeks with a simultaneous daily injection of T2 for the last 4 weeks. The results showed that T2 administration ameliorated the expression profiles of pro- and anti-inflammatory cytokines, reduced macrophage infiltration in white adipose tissue, influenced their polarization and reduced lymphocytes recruitment. Moreover, T2 improved the expression of hypoxia markers, all altered in HFD rats, and reduced angiogenesis by decreasing the pro-angiogenic miR126 expression. Additionally, T2 reduced the oxidative damage of DNA, known to be associated to the inflammatory status. This study demonstrates that T2 is able to counteract some adverse effects caused by a long-lasting HFD and to produce beneficial effects on inflammation. Irisin and SIRT1 pathway may represent a mechanism underlying the above described effects.

scholarly journals Effects of high fat diet and maternal binge-like alcohol consumption and their influence on cocaine response in female mice offspring

2020 ◽  
Author(s):  
L Duart-Castells ◽  
L Cantacorps ◽  
R López-Arnau ◽  
S Montagud-Romero ◽  
B Puster ◽  
...  
Keyword(s):  
High Fat Diet ◽  
Fetal Alcohol Spectrum Disorders ◽  
Alcohol Exposure ◽  
Female Offspring ◽  
Blood Levels ◽  
Childhood And Adolescence ◽  
Standard Diet ◽  
Neurocognitive Deficits ◽  
High Fat ◽  
Increased Risk

Abstract BACKGROUD Prenatal alcohol exposure is a leading cause of neurobehavioral and neurocognitive deficits collectively known as fetal alcohol spectrum disorders (FASD), including eating disorders and increased risk for substance abuse as very common issues. In this context, the present study aimed to assess the interaction between alcohol exposure during gestation and lactation periods (PLAE) and a high fat diet (HFD) during childhood and adolescence. METHODS Pregnant C57BL/6 mice underwent a procedure for alcohol binge drinking during gestation and lactation periods. Subsequently, PLAE female offspring were fed with a HFD for 8 weeks and thereafter, nutrition-related parameters as well as their response to cocaine were assessed. RESULTS In our model, feeding young females with a HFD increased their triglyceride blood levels but did not induce an overweight compared to those fed with a standard diet. Moreover, PLAE affected how females responded to the fatty diet as they consumed less amount of food than water-exposed offspring, consistent with a lower gain of body weight. HFD increased the psychostimulant effects of cocaine. Surprisingly, PLAE reduced the locomotor responses to cocaine without modifying cocaine-induced reward. Moreover, PLAE prevented the striatal overexpression of cannabinoid 1 receptors induced by a HFD and induced an alteration of myelin damage biomarker in the prefrontal cortex, an effect that was mitigated by a HFD-based feeding. CONCLUSION Therefore, in female offspring, some effects triggered by one of these factors, PLAE or a HFD, were blunted by the other, suggesting a close interaction between the involved mechanisms.

scholarly journals 3,5 Diiodo-l-Thyronine (T2) Promotes the Browning of White Adipose Tissue in High-Fat Diet-Induced Overweight Male Rats Housed at Thermoneutrality

Cells ◽  
2019 ◽  
Vol 8 (3) ◽  
pp. 256 ◽  
Author(s):  
Rosalba Senese ◽  
Federica Cioffi ◽  
Rita De Matteis ◽  
Giuseppe Petito ◽  
Pieter de Lange ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Fat Mass ◽  
White Adipose Tissue ◽  
High Fat Diet ◽  
Underlying Mechanism ◽  
Male Rats ◽  
Standard Diet ◽  
High Fat ◽  
Beneficial Effects ◽  
Adipose Cells

The conversion of white adipose cells into beige adipose cells is known as browning, a process affecting energy metabolism. It has been shown that 3,5 diiodo-l-thyronine (T2), an endogenous metabolite of thyroid hormones, stimulates energy expenditure and a reduction in fat mass. In light of the above, the purpose of this study was to test whether in an animal model of fat accumulation, T2 has the potential to activate a browning process and to explore the underlying mechanism. Three groups of rats were used: (i) receiving a standard diet for 14 weeks; (ii) receiving a high-fat diet (HFD) for 14 weeks; and (iii) receiving a high fat diet for 10 weeks and being subsequently treated for four weeks with an HFD together with the administration of T2. We showed that T2 was able to induce a browning in the white adipose tissue of T2-treated rats. We also showed that some miRNA (miR133a and miR196a) and MAP kinase 6 were involved in this process. These results indicate that, among others, the browning may be another cellular/molecular mechanism by which T2 exerts its beneficial effects of contrast to overweight and of reduction of fat mass in rats subjected to HFD.

scholarly journals Pathological Conversion of Mouse Perivascular Adipose Tissue by Notch Activation

2020 ◽  
Vol 40 (9) ◽  
pp. 2227-2243 ◽  
Author(s):  
Joshua M. Boucher ◽  
Larisa Ryzhova ◽  
Anne Harrington ◽  
Jessica Davis-Knowlton ◽  
Jacqueline E. Turner ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Notch Signaling ◽  
High Fat Diet ◽  
Vascular Function ◽  
Uncoupling Protein ◽  
Standard Diet ◽  
Lipid Deposition ◽  
High Fat ◽  
Perivascular Adipose Tissue ◽  
Brown Adipose

Objective: Perivascular adipose tissue (PVAT) surrounding arteries supports healthy vascular function. During obesity, PVAT loses its vasoprotective effect. We study pathological conversion of PVAT, which involves molecular changes in protein profiles and functional changes in adipocytes. Approach and Results: C57BL6/J mice were fed a 60% high-fat diet for 12 weeks or a cardioprotective 30% calorie-restricted diet for 5 weeks. Proteomic analysis identified PVAT as a molecularly distinct adipose depot, and novel markers for thermogenic adipocytes, such as GRP75 (stress-70 protein, mitochondrial), were identified. High-fat diet increased the similarity of protein signatures in PVAT and brown adipose, suggesting activation of a conserved whitening pathway. The whitening phenotype was characterized by suppression of UCP1 (uncoupling protein 1) and increased lipid deposition, leptin, and inflammation, and specifically in PVAT, elevated Notch signaling. Conversely, PVAT from calorie-restricted mice had decreased Notch signaling and less lipid. Using the Adipoq-Cre strain, we constitutively activated Notch1 signaling in adipocytes, which phenocopied the changes in PVAT caused by a high-fat diet, even on a standard diet. Preadipocytes from mouse PVAT expressed Sca1, CD140a, Notch1, and Notch2, but not CD105, showing differences compared with preadipocytes from other depots. Inhibition of Notch signaling during differentiation of PVAT-derived preadipocytes reduced lipid deposition and adipocyte marker expression. Conclusions: PVAT shares features with other adipose depots, but has a unique protein signature that is regulated by dietary stress. Increased Notch signaling in PVAT is sufficient to initiate the pathological conversion of PVAT by promoting adipogenesis and lipid accumulation and may thus prime the microenvironment for vascular disease.

scholarly journals Gab2 deficiency suppresses high-fat diet-induced obesity by reducing adipose tissue inflammation and increasing brown adipose function in mice

2021 ◽  
Vol 12 (2) ◽  
Author(s):  
Xinhui Wang ◽  
Yinan Zhao ◽  
Dekun Zhou ◽  
Yingpu Tian ◽  
Gensheng Feng ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
High Fat Diet ◽  
Scaffolding Protein ◽  
Regulation Mechanism ◽  
Standard Diet ◽  
High Fat ◽  
Diet Induced Obesity ◽  
Brown Adipose ◽  
Relevant Regulation

AbstractObesity is caused by a long-term imbalance between energy intake and consumption and is regulated by multiple signals. This study investigated the effect of signaling scaffolding protein Gab2 on obesity and its relevant regulation mechanism. Gab2 knockout (KO) and wild-type (WT) mice were fed with a standard diet (SD) or high-fat diet (HFD) for 12 weeks. The results showed that the a high-fat diet-induced Gab2 expression in adipose tissues, but deletion of Gab2 attenuated weight gain and improved glucose tolerance in mice fed with a high-fat diet. White adipose tissue and systemic inflammations were reduced in HFD-fed Gab2 deficiency mice. Gab2 deficiency increased the expression of Ucp1 and other thermogenic genes in brown adipose tissue. Furthermore, the regulation of Gab2 on the mature differentiation and function of adipocytes was investigated in vitro using primary or immortalized brown preadipocytes. The expression of brown fat-selective genes was found to be elevated in differentiated adipocytes without Gab2. The mechanism of Gab2 regulating Ucp1 expression in brown adipocytes involved with its downstream PI3K (p85)-Akt-FoxO1 signaling pathway. Our research suggests that deletion of Gab2 suppresses diet-induced obesity by multiple pathways and Gab2 may be a novel therapeutic target for the treatment of obesity and associated complications.

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