Effects of a High-Fat Diet on Tissue Mass, Bone, and Glucose Tolerance after Chronic Complete Spinal Cord Transection in Male Mice

Neurotrauma Reports, 2020 · DOI: 10.1089/neur.2020.0014 · Published: January 1, 2020

Spinal Cord Injury Endocrinology Nutrition & Dietetics

Simple Explanation

This study investigates how a high-fat diet affects mice after spinal cord injury (SCI), focusing on glucose tolerance, tissue mass, and bone health. The researchers compared mice with SCI to those without, feeding some a high-fat diet and others a standard diet, then measuring glucose levels, tissue weights, and bone density. The findings suggest that a high-fat diet worsens glucose tolerance after SCI, even when fat mass is reduced, and that SCI leads to bone loss regardless of diet.

Study Duration

84 days

Participants

Male C57BL/6 mice

Evidence Level

Animal study

Key Findings

1
SCI animals display signs of glucose intolerance at 84 days after initiating HFD despite a decrease in body mass and lower iFAT, eFAT, and oFAT masses.
2
SCI reduced the mass of hindlimb muscle, eFAT, oFAT, and iFAT and HFD did not alter this effect.
3
SCI produced cancellous and cortical bone loss and HFD did not alter this effect.

Research Summary

This study examined the effects of a high-fat diet (HFD) on glucose tolerance, tissue mass, and bone after spinal cord injury (SCI) in mice. SCI mice fed a HFD showed glucose intolerance, reduced muscle and fat mass, and decreased liver weight compared to controls. SCI also led to bone loss irrespective of diet. The findings suggest that HFD may serve as a model to study insulin resistance post-SCI, independent of obesity, but caution is needed when translating these results to human SCI populations due to differences in body composition changes.

Practical Implications

Model for Insulin Resistance

The HFD-fed SCI mouse model may help researchers understand the mechanisms of insulin resistance and T2DM development after SCI.

Therapeutic Targets

Identifying the cellular and molecular changes in fat and carbohydrate metabolism post-SCI could lead to targeted therapies.

Clinical Caution

Findings from this mouse model may not directly translate to human SCI patients due to differences in body composition changes, highlighting the need for further research.

Study Limitations

1
Decrease in fatty tissues in SCI mice limits clinical translation of the findings.
2
A spinal cord transection was used that does not fully recapitulate the more common complex clinical lesion.
3
We did not make formal recordings of food intake, so it is possible that some of the outcomes we note are due to altered caloric intake.

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