A mechanistic examination of the impact of maternal high-fat diet on long-term offspring obesity risk.

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.

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060. OVER FEEDING EARLY IN LIFE AND RISK OF OBESITY: INSIGHT FROM THE RODENT

Reproduction Fertility and Development ◽

10.1071/srb09abs060 ◽

2009 ◽

Vol 21 (9) ◽

pp. 15

Author(s):

M. J. Morris

Keyword(s):

High Fat Diet ◽

Animal Studies ◽

Energy Homeostasis ◽

Maternal Obesity ◽

Obesity Risk ◽

High Fat ◽

Generational Effects ◽

Hypothalamic Regulation ◽

The Impact ◽

Detrimental Impact

While adult lifestyle factors undoubtedly contribute to the incidence of obesity and its attendant disorders, mounting evidence suggests that programming of obesity may occur following over-nutrition during development. As hypothalamic control of appetite and energy expenditure is set early in life and can be perturbed by certain exposures such as under-nutrition and altered metabolic and hormonal signals, in utero exposure to maternal obesity related changes may contribute to programming of obesity in offspring. Data from animal studies indicate both intrauterine and postnatal environments are critical determinants of the development of pathways regulating energy homeostasis. Experimental evidence in rat studies from our laboratory points to an additive detrimental impact of high fat diet consumption after weaning in animals born of obese mothers. Deleterious effects of high fat diet during pregnancy on metabolic profile, adiposity and cardiac hypertrophy were enhanced by postnatal over consumption. Even modest early postnatal overfeeding induced by litter size reduction leads to increased adiposity. Studies are needed to determine to what extent the effect of maternal and early nutritional changes persist. This presentation summarizes recent evidence of the impact of maternal obesity on subsequent obesity risk, paying particular attention to the hypothalamic regulation of appetite, and markers of metabolic control. There is an urgent need to investigate the mechanisms underlying the trans-generational effects of maternal obesity due to an extraordinary rise in the rates of maternal obesity.

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The impact of High Fat Diet on bone: potential mechanisms

Food & Function ◽

10.1039/d0fo02664f ◽

2021 ◽

Author(s):

Qiao Jie ◽

Yue-Zhong Ren ◽

Yi-wen Wu

Keyword(s):

Total Energy ◽

High Fat Diet ◽

High Fat ◽

High Fat Diets ◽

Fat Diets ◽

The Impact

High-fat diets(HFD)are defined as lipids accounting for exceeded 30% of total energy in-take, and current research is mostly 45% and 60%. With a view of the tendency that patients who...

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The beneficial effects of Lactobacillus fermented black barley on high fat diet-induced fatty liver in rats

Food & Function ◽

10.1039/d1fo00290b ◽

2021 ◽

Author(s):

Qi Guan ◽

Xinwen Ding ◽

Lingyue Zhong ◽

Chuang Zhu ◽

Pan Nie ◽

...

Keyword(s):

Fatty Liver ◽

High Fat Diet ◽

Metabolic Disorders ◽

High Fat ◽

Beneficial Effects ◽

Phytochemical Composition

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...

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A Newly Developed Synbiotic Yogurt Prevents Diabetes by Improving the Microbiome–Intestine–Pancreas Axis

International Journal of Molecular Sciences ◽

10.3390/ijms22041647 ◽

2021 ◽

Vol 22 (4) ◽

pp. 1647

Author(s):

Brandi Miller ◽

Rabina Mainali ◽

Ravinder Nagpal ◽

Hariom Yadav

Keyword(s):

High Fat Diet ◽

Microbiota Composition ◽

Preventive Strategies ◽

Human Origin ◽

High Fat ◽

Diabetes In Mice ◽

Diabetes Progression ◽

Gut Microbiota Composition

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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