Event Title

The Effect of β-hydroxy-β-methylbutyrate (HMB) on C2C12 Cells

Presenter Information

Alyssa Altheimer, Oberlin College

Location

Science Center, Bent Corridor

Start Date

10-27-2017 6:00 PM

End Date

10-27-2017 6:40 PM

Research Program

Baylor College of Medicine Summer Medical and Research Training (SMART) Program

Poster Number

39

Abstract

Malnutrition during the neonatal period can lead to a lifelong reduction in muscle mass. This effect can be attributed to a loss of muscle stem cells (satellite cells) and a blunted recovery of protein and satellite cells following nutritional rehabilitation. The leucine metabolite β-hydroxy-β-methylbutyrate (HMB), a dietary supplement currently used to promote skeletal muscle hypertrophy, shows promise as an intervention to reverse this muscle deficit. However, the mechanism by which HMB causes these effects is uncertain. This summer, I used C2C12 cells (immortalized mouse satellite cells) to study the effect of HMB on satellite cells, with the goal of later testing satellite cells harvested from undernourished and control mice. My hypothesis was that HMB would stimulate cell proliferation and expression of myogenic genes associated with proliferation, but not differentiation, in a dose-dependent manner. Cell counts and qPCR mRNA analyses suggested that the HMB did not stimulate, and may have inhibited, cell proliferation, contrary to my hypothesis. However, I used a commercial HMB preparation containing other ingredients that may have been cytotoxic to the cells. The next step is to repeat the experiment with pure HMB and then to apply the procedure I developed to satellite cells from undernourished and control mice.

Major

Biochemistry

Project Mentor(s)

Marta Fiorotto, Eric Meadows and Ryan Fleischmann, Children's Nutrition Research Center, Baylor College of Medicine

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Oct 27th, 6:00 PM Oct 27th, 6:40 PM

The Effect of β-hydroxy-β-methylbutyrate (HMB) on C2C12 Cells

Science Center, Bent Corridor

Malnutrition during the neonatal period can lead to a lifelong reduction in muscle mass. This effect can be attributed to a loss of muscle stem cells (satellite cells) and a blunted recovery of protein and satellite cells following nutritional rehabilitation. The leucine metabolite β-hydroxy-β-methylbutyrate (HMB), a dietary supplement currently used to promote skeletal muscle hypertrophy, shows promise as an intervention to reverse this muscle deficit. However, the mechanism by which HMB causes these effects is uncertain. This summer, I used C2C12 cells (immortalized mouse satellite cells) to study the effect of HMB on satellite cells, with the goal of later testing satellite cells harvested from undernourished and control mice. My hypothesis was that HMB would stimulate cell proliferation and expression of myogenic genes associated with proliferation, but not differentiation, in a dose-dependent manner. Cell counts and qPCR mRNA analyses suggested that the HMB did not stimulate, and may have inhibited, cell proliferation, contrary to my hypothesis. However, I used a commercial HMB preparation containing other ingredients that may have been cytotoxic to the cells. The next step is to repeat the experiment with pure HMB and then to apply the procedure I developed to satellite cells from undernourished and control mice.