scholarly journals Administration of the Antioxidant N-Acetyl-Cysteine in Pregnant Mice Has Long-Term Positive Effects on Metabolic and Behavioral Endpoints of Male and Female Offspring Prenatally Exposed to a High-Fat Diet

Author(s):  
Alessandra Berry ◽  
Veronica Bellisario ◽  
Pamela Panetta ◽  
Carla Raggi ◽  
Maria C. Magnifico ◽  
...  
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 ◽  
...  

2020 ◽  
Vol 11 (9) ◽  
pp. 8193-8201
Author(s):  
Wenjin Guo ◽  
Juxiong Liu ◽  
Shuang Hou ◽  
Guiqiu Hu ◽  
He Ma ◽  
...  

Long-term intake of a high-fat diet seriously affects the health of pregnant women and leads to increased levels of inflammation in the mammary gland.


2010 ◽  
Vol 26 (3) ◽  
pp. 291-302 ◽  
Author(s):  
Antònia Nadal-Casellas ◽  
Emilia Amengual-Cladera ◽  
Ana María Proenza ◽  
Isabel Lladó ◽  
Magdalena Gianotti

2007 ◽  
Vol 293 (1) ◽  
pp. E121-E131 ◽  
Author(s):  
Michelle Lee ◽  
Andrea Kim ◽  
Streamson C. Chua ◽  
Silvana Obici ◽  
Sharon L. Wardlaw

To determine whether long-term melanocortinergic activation can attenuate the metabolic effects of a high fat diet, mice overexpressing an NH2-terminal POMC transgene that includes α- and γ3-MSH were studied on either a 10% low-fat diet (LFD) or 45% high-fat diet (HFD). Weight gain was modestly reduced in transgenic (Tg-MSH) male and female mice vs. wild type (WT) on HFD ( P < 0.05) but not LFD. Substantial reductions in body fat percentage were found in both male and female Tg-MSH mice on LFD ( P < 0.05) and were more pronounced on HFD ( P < 0.001). These changes occurred in the absence of significant feeding differences in most groups, consistent with effects of Tg-MSH on energy expenditure and partitioning. This is supported by indirect calorimetry studies demonstrating higher resting oxygen consumption and lower RQ in Tg-MSH mice on the HFD. Tg-MSH mice had lower fasting insulin levels and improved glucose tolerance on both diets. Histological and biochemical analyses revealed that hepatic fat accumulation was markedly reduced in Tg-MSH mice on the HFD. Tg-MSH also attenuated the increase in corticosterone induced by the HFD. Higher levels of Agrp mRNA, which might counteract effects of the transgene, were measured in Tg-MSH mice on LFD ( P = 0.02) but not HFD. These data show that long-term melanocortin activation reduces body weight, adiposity, and hepatic fat accumulation and improves glucose metabolism, particularly in the setting of diet-induced obesity. Our results suggest that long-term melanocortinergic activation could serve as a potential strategy for the treatment of obesity and its deleterious metabolic consequences.


2019 ◽  
Vol 2 (1) ◽  
Author(s):  
Weston He ◽  
Trupti Trivedi ◽  
Gabriel Pagnotti ◽  
Sreemala Murthy ◽  
Yun She ◽  
...  

Background and Hypothesis: Hyperglycemia is a major source of disease and morbidity among the adult population. Prior studies correlate long-term high fat diet (HFD) mediated hyperglycemia with bone fragility and muscle weakness. Furthermore, the mechanism driving hyperglycemia between sexes are unknown. Our group previously showed that HFDs induced insulin resistance in male mice and glucose intolerance in female mice. This establishes the need to study the impact of long-term HFDs on the bones and muscles using an older cohort of both male and female mice. For that, we hypothesized a long-term HFD mediated hyperglycemia will change bone and muscle structures and impair their functions in adult male and female mice. Experimental Design or Project Methods: 22-week C57Bl6 mice were fed either a HFD or low fat diet (LFD) for 25 weeks. After euthanasia, bones and muscles were harvested and evaluated using MicroCT, histology, and mechanical testing. Statistical analysis was performed using GraphPad Prism with p<0.05 considered significant. Results: MicoCT data saw significant reductions to cortical thickness (p<0.05), bone mineral density (p<0.001), and increases to medullary area (p<0.05) among HFD males and females compared to LFD. HFD-males also experienced significant increase in cortical porosity (P<0.001) whereas no changes were noted in HFDfemales. Trabecular bone volume was relatively unchanged. HFD increased cortical osteoclast surface (p<0.001) for both sexes. Bone histology saw increased marrow adiposity among HFD-females (p<0.05). Muscle histology exhibited HFD-related reductions in myofiber diameter (p<0.001) for both sexes. Mechanical testing demonstrated reduced young’s modulus (p<0.05) and yield stress (p<0.05) among HFD mice, despite non-significant differences in ultimate strength. Conclusion and Potential Impact: The changes associated with a long-term HFD differed between sexes but still led to functional impairments of bone and muscle for both sexes, emphasizing the importance of looking further into the mechanisms responsible for these changes. This can potentially translate to the clinic in the treatment of musculoskeletal complications associated with HFDs.


Metabolites ◽  
2020 ◽  
Vol 10 (11) ◽  
pp. 462
Author(s):  
Santiago Guerra-Cantera ◽  
Laura M. Frago ◽  
María Jiménez-Hernaiz ◽  
Purificación Ros ◽  
Alejandra Freire-Regatillo ◽  
...  

The insulin-like growth factor (IGF) system is responsible for growth, but also affects metabolism and brain function throughout life. New IGF family members (i.e., pappalysins and stanniocalcins) control the availability/activity of IGFs and are implicated in growth. However, how diet and obesity modify this system has been poorly studied. We explored how intake of a high-fat diet (HFD) or commercial control diet (CCD) affects the IGF system in the circulation, visceral adipose tissue (VAT) and hypothalamus. Male and female C57/BL6J mice received HFD (60% fat, 5.1 kcal/g), CCD (10% fat, 3.7 kcal/g) or chow (3.1 % fat, 3.4 kcal/g) for 8 weeks. After 7 weeks of HFD intake, males had decreased glucose tolerance (p < 0.01) and at sacrifice increased plasma insulin (p < 0.05) and leptin (p < 0.01). Circulating free IGF1 (p < 0.001), total IGF1 (p < 0.001), IGF2 (p < 0.05) and IGFBP3 (p < 0.01) were higher after HFD in both sexes, with CCD increasing IGFBP2 in males (p < 0.001). In VAT, HFD reduced mRNA levels of IGF2 (p < 0.05), PAPP-A (p < 0.001) and stanniocalcin (STC)-1 (p < 0.001) in males. HFD increased hypothalamic IGF1 (p < 0.01), IGF2 (p < 0.05) and IGFBP5 (p < 0.01) mRNA levels, with these changes more apparent in females. Our results show that diet-induced changes in the IGF system are tissue-, sex- and diet-dependent.


2009 ◽  
Vol 297 (3) ◽  
pp. E708-E716 ◽  
Author(s):  
Emil Egecioglu ◽  
Karolina Ploj ◽  
Xiufeng Xu ◽  
Mikael Bjursell ◽  
Nicolas Salomé ◽  
...  

To investigate the role of the central neuromedin U (NMU) signaling system in body weight and energy balance regulation, we examined the effects of long-term intracerebroventricular (icv) infusion of NMU in C57Bl/6 mice and in mice lacking the gene encoding NMU receptor 2. In diet-induced obese male and female C57BL/6 mice, icv infusion of NMU (8 μg·day−1·mouse−1) for 7 days decreased body weight and total energy intake compared with vehicle treatment. However, these parameters were unaffected by NMU treatment in lean male and female C57BL/6 mice fed a standard diet. In addition, female (but not male) NMUR2-null mice had increased body weight and body fat mass when fed a high-fat diet but lacked a clear body weight phenotype when fed a standard diet compared with wild-type littermates. Furthermore, female (but not male) NMUR2-null mice fed a high-fat diet were protected from central NMU-induced body weight loss compared with littermate wild-type mice. Thus, we provide the first evidence that long-term central NMU treatment reduces body weight, food intake, and adiposity and that central NMUR2 signaling is required for these effects in female but not male mice.


2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Renato S. Gaspar ◽  
Amanda J. Unsworth ◽  
Alaa Al-Dibouni ◽  
Alexander P. Bye ◽  
Tanya Sage ◽  
...  

AbstractMaternal over-nutrition increases the risk of diabetes and cardiovascular events in offspring. While prominent effects on cardiovascular health are observed, the impact on platelet physiology has not been studied. Here, we examined whether maternal high-fat diet (HF) ingestion affects the platelet function in lean and obese offspring. C57BL6/N mice dams were given a HF or control (C) diet for 8 weeks before and during pregnancy. Male and female offspring received C or HF diets for 26 weeks. Experimental groups were: C/C, dam and offspring fed standard laboratory diet; C/HF dam fed standard laboratory diet and offspring fed HF diet; HF/C and HF/HF. Phenotypic and metabolic tests were performed and blood collected for platelet studies. Compared to C/C, offspring HF groups were obese, with fat accumulation, hyperglycaemia and insulin resistance. Female offspring did not present platelet hyperactivity, hence we focused on male offspring. Platelets from HF/HF mice were larger, hyperactive and presented oxidative stress when compared to C/C. Maternal and offspring HF diet results in platelet hyperactivation in male mouse offspring, suggesting a novel ‘double-hit’ effect.


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