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Moore, B. T.

Publications and source records attributed to Moore, B. T..

2 recordsLinked to original sources

MUSCLE MITOCHONDRIAL CAPACITY AND ENDURANCE IN ADULTS WITH TYPE 1 DIABETES

The impact of type 1 diabetes (T1D) on muscle endurance and oxidative capacity is currently unknown. PurposeMeasure muscle endurance and oxidative capacity of adults with T1D compared to controls. MethodsA cross-sectional study design with a control group was used. Subjects (19-37 years old) with T1D (n=17) and controls (n=17) were assessed with hemoglobin A1c (HbA1c) and casual glucose. Muscle endurance was measured with an accelerometer at stimulation frequencies of 2, 4, and 6 Hz for a total of nine minutes. Mitochondrial capacity was measured using near-infrared spectroscopy after exercise as the rate constant of the rate of recovery of oxygen consumption. ResultsT1D and control groups were similar in age, sex, height, and race. The T1D group had slightly higher BMI values and adipose tissue thickness over the forearm muscles. Casual glucose was 150{+/-}70 mg/dL for T1D and 98{+/-}16 mg/dL for controls (P=0.006). HbA1c of T1D subjects was 7.1{+/-}0.9% and 5.0{+/-}0.4% for controls (P<0.01). Endurance indexes at 2, 4, and 6 Hz were 94.5{+/-}5.2%, 81.8{+/-}8.4%, and 68.6{+/-}13.5% for T1D and 94.6{+/-}4.1%, 85.9{+/-}6.3%, and 68.7{+/-}15.4% for controls (p = 0.97, 0.12, 0.99, respectively). There were no differences between groups in mitochondrial capacity (T1D= 1.9{+/-}0.5 min-1 and control=1.8{+/-}0.4 min-1, P=0.29) or reperfusion rate (T1D= 8.8{+/-}2.8s and control=10.3{+/-}3.0s, P=0.88). There were no significant correlations between HbA1c and either muscle endurance, mitochondrial capacity or reperfusion rate. ConclusionsAdults with T1D did not have reduced oxidative capacity, muscle endurance or muscle reperfusion rates compared to controls. HbA1c also did not correlate with muscle endurance, mitochondrial capacity or reperfusion rates. Future studies should extend these measurements to older people or people with poorly-controlled T1D.

physiology↗

Population selection and sequencing of C. elegans wild isolates identifies a region on chromosome III affecting starvation resistance

To understand the genetic basis of complex traits, it is important to be able to efficiently phenotype many genetically distinct individuals. In the nematode Caenorhabditis elegans, individuals have been isolated from diverse populations around the globe and whole-genome sequenced. As a result, hundreds of wild strains with known genome sequences can be used for genome-wide association studies (GWAS). However, phenotypic analysis of these strains can be laborious, particularly for quantitative traits requiring multiple measurements per strain. Starvation resistance is likely a fitness-proximal trait for nematodes, and it is related to metabolic disease risk in humans. However, natural variation in C. elegans starvation resistance has not been characterized, and precise measurement of the trait is time-intensive. Here, we developed a population selection and sequencing-based approach to phenotype starvation resistance in a pool of 96 wild strains. We used restriction site-associated DNA sequencing (RAD-seq) to infer the frequency of each strain among survivors in a mixed culture over time during starvation. We used manual starvation survival assays to validate the trait data, confirming that strains that increased in frequency over time are starvation-resistant relative to strains that decreased in frequency. These results document natural variation in starvation resistance. Further, we found that variation in starvation resistance is significantly associated with variation at a region on chromosome III. Using a near-isogenic line (NIL), we showed the importance of this genomic interval for starvation resistance. This study demonstrates the feasibility of using population selection and sequencing in an animal model for phenotypic analyses of quantitative traits, reveals natural variation of starvation resistance in C. elegans, and identifies a genomic region that contributes to such variation.

genetics↗