scholarly journals Sex-specific effects of metformin and liraglutide on renal pathology and expression of connexin 45 and pannexin 1 following long-term high-fat high-sugar diet

2021 ◽  
Vol 123 (8) ◽  
pp. 151817
Author(s):  
Martina Luetić ◽  
Genia Kretzschmar ◽  
Maximilian Grobe ◽  
Leo Jerčić ◽  
Ivana Bota ◽  
...  
2015 ◽  
Vol 93 (4) ◽  
pp. 1641-1655 ◽  
Author(s):  
C. Hue-Beauvais ◽  
E. Koch ◽  
P. Chavatte-Palmer ◽  
L. Galio ◽  
S. Chat ◽  
...  

2021 ◽  
Vol 12 ◽  
Author(s):  
Vanessa Caruline Araujo-Silva ◽  
Alice Santos-Silva ◽  
Andressa Silva Lourenço ◽  
Cristielly Maria Barros-Barbosa ◽  
Rafaianne Queiroz Moraes-Souza ◽  
...  

Embryo-fetal exposure to maternal disorders during intrauterine life programs long-term consequences for the health and illness of offspring. In this study, we evaluated whether mild diabetic rats that were given high-fat/high-sugar (HF/HS) diet presented maternal and fetal changes at term pregnancy. Female rats received citrate buffer (non-diabetic-ND) or streptozotocin (diabetic-D) after birth. According to the oral glucose tolerance test (OGTT), the experimental groups (n = 11 animals/group) were composed of non-diabetic and diabetic receiving standard diet (S) or HF/HS diet. High-fat/high-sugar diet (30% kcal of lard) in chow and water containing 5% sucrose and given 1 month before mating and during pregnancy. During and at the end of pregnancy, obesity and diabetes features were determined. After laparotomy, blood samples, periovarian fat, and uterine content were collected. The diabetic rats presented a higher glycemia and percentage of embryonic losses when compared with the NDS group. Rats DHF/HS presented increased obesogenic index, caloric intake, and periovarian fat weight and reduced gravid uterus weight in relation to the other groups. Besides, this association might lead to the inflammatory process, confirmed by leukocytosis. Obese rats (NDHF/HS and DHF/HS) showed higher triglyceride levels and their offspring with lower fetal weight and ossification sites, indicating intrauterine growth restriction. This finding may contribute to vascular alterations related to long-term hypertensive disorders in adult offspring. The fetuses from diabetic dams showed higher percentages of skeletal abnormalities, and DHF/HS dams still had a higher rate of anomalous fetuses. Thus, maternal diabetes and/or obesity induces maternal metabolic disorders that contribute to affect fetal development and growth.


2016 ◽  
Vol 7 ◽  
Author(s):  
Jon-Philippe K. Hyatt ◽  
Lisa Nguyen ◽  
Allison E. Hall ◽  
Ashley M. Huber ◽  
Jessica C. Kocan ◽  
...  

2013 ◽  
Vol 110 (11) ◽  
pp. 2069-2083 ◽  
Author(s):  
Diane Hosking ◽  
Vanessa Danthiir

Dietary patterns derived from factor analytic procedures have been demonstrated to predict demographic and health outcomes across a wide range of populations. To examine the potential utility of long-term dietary recall, in the present study, we examined associations between dietary patterns from across the lifespan and demographic and later-life cardiovascular-related health variables, using the Lifetime Diet Questionnaire (LDQ). The LDQ is a self-administered, non-quantitative, retrospective FFQ designed to assess dietary intake from childhood to older age. Participants (n 352) from the Older People, Omega-3 and Cognitive Health trial, aged 65–91 years, completed the LDQ. Exploratory factor analysis was conducted on the LDQ and plausible dietary patterns were derived. As a result, three patterns were extracted from each life period, with five distinct patterns overall; these were ‘traditional Australian’ and ‘non-traditional Australian’, ‘high-sugar and high-fat’, ‘vegetable’ and ‘fruit and vegetable’ patterns. In separate adjusted regression models, age, sex, education, income, parental background and childhood physical activity all significantly predicted dietary patterns across the lifespan. A ‘traditional Australian’ pattern in childhood predicted higher HDL-cholesterol levels and lower odds of cholesterol medication use; lower HDL-cholesterol levels were predicted by the adult ‘processed, high-sugar and high-fat’ pattern, and higher intake of a ‘non-traditional Australian’ pattern in adulthood also predicted lower odds of using cardiac medications. Lifetime dietary recall, as instantiated by the LDQ, provides a hitherto untapped source of long-term dietary information in older adults that may contribute to greater understanding of the impact exerted by early-life and cumulative dietary choices on later-life health.


Cells ◽  
2021 ◽  
Vol 10 (11) ◽  
pp. 2805
Author(s):  
Tiziana Napolitano ◽  
Fabio Avolio ◽  
Serena Silvano ◽  
Sara Forcisi ◽  
Anja Pfeifer ◽  
...  

Background: Although several approaches have revealed much about individual factors that regulate pancreatic development, we have yet to fully understand their complicated interplay during pancreas morphogenesis. Gfi1 is transcription factor specifically expressed in pancreatic acinar cells, whose role in pancreas cells fate identity and specification is still elusive. Methods: In order to gain further insight into the function of this factor in the pancreas, we generated animals deficient for Gfi1 specifically in the pancreas. Gfi1 conditional knockout animals were phenotypically characterized by immunohistochemistry, RT-qPCR, and RNA scope. To assess the role of Gfi1 in the pathogenesis of diabetes, we challenged Gfi1-deficient mice with two models of induced hyperglycemia: long-term high-fat/high-sugar feeding and streptozotocin injections. Results: Interestingly, mutant mice did not show any obvious deleterious phenotype. However, in depth analyses demonstrated a significant decrease in pancreatic amylase expression, leading to a diminution in intestinal carbohydrates processing and thus glucose absorption. In fact, Gfi1-deficient mice were found resistant to diet-induced hyperglycemia, appearing normoglycemic even after long-term high-fat/high-sugar diet. Another feature observed in mutant acinar cells was the misexpression of ghrelin, a hormone previously suggested to exhibit anti-apoptotic effects on β-cells in vitro. Impressively, Gfi1 mutant mice were found to be resistant to the cytotoxic and diabetogenic effects of high-dose streptozotocin administrations, displaying a negligible loss of β-cells and an imperturbable normoglycemia. Conclusions: Together, these results demonstrate that Gfi1 could turn to be extremely valuable for the development of new therapies and could thus open new research avenues in the context of diabetes research.


2021 ◽  
Author(s):  
Qi Guan ◽  
Xinwen Ding ◽  
Lingyue Zhong ◽  
Chuang Zhu ◽  
Pan Nie ◽  
...  

Long term high-fat diet (HF) can cause metabolic disorders, which might induce fatty liver. Fermented whole cereal food exhibit healthy potential due to their unique phytochemical composition and probiotics. In...


2021 ◽  
Vol 22 (4) ◽  
pp. 1647
Author(s):  
Brandi Miller ◽  
Rabina Mainali ◽  
Ravinder Nagpal ◽  
Hariom Yadav

The prevalence of type 2 diabetes mellitus (T2D) is increasing worldwide, and there are no long-term preventive strategies to stop this growth. Emerging research shows that perturbations in the gut microbiome significantly contribute to the development of T2D, while microbiome modulators may be beneficial for T2D prevention. However, microbiome modulators that are effective, safe, affordable, and able to be administered daily are not yet available. Based on our previous pro- and prebiotic studies, we developed a novel synbiotic yogurt comprised of human-origin probiotics and plant-based prebiotics and investigated its impact on diet- and streptozotocin-induced T2D in mice. We compared the effects of our synbiotic yogurt to those of a commercially available yogurt (control yogurt). Interestingly, we found that the feeding of the synbiotic yogurt significantly reduced the development of hyperglycemia (diabetes) in response to high-fat diet feeding and streptozotocin compared to milk-fed controls. Surprisingly, the control yogurt exacerbated diabetes progression. Synbiotic yogurt beneficially modulated the gut microbiota composition compared to milk, while the control yogurt negatively modulated it by significantly increasing the abundance of detrimental bacteria such as Proteobacteria and Enterobacteriaceae. In addition, the synbiotic yogurt protected pancreatic islet morphology compared to the milk control, while the control yogurt demonstrated worse effects on islets. These results suggest that our newly developed synbiotic yogurt protects against diabetes in mice and can be used as a therapeutic to prevent diabetes progression.


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