Daniel Fernandes’s research while affiliated with Vanderbilt University and other places

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Publications (1)

Age-related changes in body mass and non-fasting glucose before and after switching male mice from standard chow to 1 of 2 purified diets (medial ± IQR). A While the mice consumed a standard rodent chow, there were no pronounced differences in body mass between the 2 strains. When the mice started to consume a synthetic diet at 16 weeks of age, high fat increased body mass, but this depended on the strain. B From 11 to 16 weeks of age, a few mice had circulating levels above 250 mg/dl, but this was not consistent as they matured. Corresponding to the consumption of the high fat diet, all NONcNZ010/LtJ mice had glucose levels well above 250 mg/dl, while glucose levels increased for some NON/ShiLtJ mice
Representative μCT images of the distal femur metaphysis from each group. In longitudinal sections of the metaphysis, there appear to be fewer trabeculae in mice fed a high fat diet for 21 weeks, irrespective of strain
Effect of diet and strain on advanced glycation end-products (AGEs). A The concentration of the AGE crosslink pentosidine was higher in the diabetic NZO10 mice than in the control ShiLtJ mice. B However, there were no significant differences in AGEs among the 4 groups when measured by fluorescence
Strain- and diet-related differences in the L6 vertebral body (VB). A As determined by μCT evaluations, the trabecular bone fraction was lower in the NZO10 mice than in the ShiLtJ mice but wasn’t affected by diet. B This was also the case for tissue mineral density of the trabecular bone in the centrum. C Despite the lack of diet effect on trabecular bone, HFD lowered the compressive strength of the VB with this mechanical property being lower in NZO10 strain than the control strain. D This effect on strength could be due to low cross-sectional area of the VB in mice fed a HFD. Tukey’s outliers, 1.5 × the interquartile range, are included in the statistical analysis
Structure and bending strength of femur mid-diaphysis. A In representative μCT cross-sectional images, the distance between the neutral axis (i.e., centroid) and the bone surface in direction of loading in three-point bending tests (i.e., cmin) appears greater in the ShiLtJ control mice than the NZO10 diabetic mice. Less apparent is the smaller cortical thickness in NZO10 mice compared ShiLtJ mice as seen representative μCT longitudinal images. B In linear regression analysis of yield moment of femur mid-diaphysis vs. section modulus (Imin/cmin), HFD significantly lowers the regression line such that the cortical bone is weaker in bending for a given section modulus (left). This was not the case for ultimate moment in bending of the femur mid-diaphysis (right)
Bone Fragility in High Fat Diet-induced Obesity is Partially Independent of Type 2 Diabetes in Mice
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  • Full-text available

July 2024

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48 Reads

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1 Citation

Calcified Tissue International

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Amy Creecy

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Daniel Fernandes

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Jeffry S. Nyman

Obesity and type 2 diabetes (T2D) are risk factors for fragility fractures. It is unknown whether this elevated risk is due to a diet favoring obesity or the diabetes that often occurs with obesity. Therefore, we hypothesized that the fracture resistance of bone is lower in mice fed with a high fat diet (45% kcal; HFD) than in mice that fed on a similar, control diet (10% kcal; LFD), regardless of whether the mice developed overt T2D. Sixteen-week-old, male NON/ShiLtJ mice (resistant to T2D) and age-matched, male NONcNZO10/LtJ (prone to T2D) received a control LFD or HFD for 21 weeks. HFD increased the bodyweight to a greater extent in the ShiLtJ mice compared to the NZO10 mice, while blood glucose levels were significantly higher in NZO10 than in ShiLtJ mice. As such, the glycated hemoglobin A1c (HbA1c) levels exceeded 10% in NZO10 mice, but it remained below 6% in ShiLtJ mice. Diet did not affect HbA1c. HFD lowered trabecular number and bone volume fraction of the distal femur metaphysis (micro-computed tomography or μCT) in both strains. For the femur mid-diaphysis, HFD significantly reduced the yield moment (mechanical testing by three-point bending) in both strains but did not affect cross-sectional bone area, cortical thickness, nor cortical tissue mineral density (μCT). Furthermore, the effect of diet on yield moment was independent of the structural resistance of the femur mid-diaphysis suggesting a negative effect of HFD on characteristics of the bone matrix. However, neither Raman spectroscopy nor assays of advanced glycation end-products identified how HFD affected the matrix. HFD also lowered the resistance of cortical bone to crack growth in only the diabetic NZO10 mice (fracture toughness testing of other femur), while HFD reduced the ultimate force of the L6 vertebra in both strains (compression testing). In conclusion, the HFD-related decrease in bone strength can occur in mice resistant and prone to diabetes indicating that a diet high in fat deleteriously affects bone without necessarily causing hyperglycemia.

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Citations (1)

... Establishing a comprehensive model of GS is crucial, as it allows for a deeper investigation into the molecular and physiological pathways altered by AGEs, providing insights that are vital for developing interventions to counteract aging and related diseases. This gap highlights the critical need for more representative models that can accurately reflect the variety and complexity of GS encountered in everyday human consumption [2,16,19,20]. ...

Reference:

WormCNN-Assisted Establishment and Analysis of Glycation Stress Models in C. elegans: Insights into Disease and Healthy Aging
Bone Fragility in High Fat Diet-induced Obesity is Partially Independent of Type 2 Diabetes in Mice

Calcified Tissue International

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Amy Creecy

·

Daniel Fernandes

·

[...]

·

Jeffry S. Nyman