Cushing’s syndrome: a model for sarcopenic obesity
Adult
Male
Sarcopenia
Matched-Pair Analysis
10265 Clinic for Endocrinology and Diabetology
610 Medicine & health
Models, Biological
Body Mass Index
03 medical and health sciences
0302 clinical medicine
Germany
Glucose Intolerance
Humans
Obesity
Prospective Studies
Muscle, Skeletal
Propensity Score
Cushing Syndrome
Glycated Hemoglobin
2. Zero hunger
Sarcopenic obesity
Frailty
Hand Strength
Middle Aged
1310 Endocrinology
3. Good health
2712 Endocrinology, Diabetes and Metabolism
Cushing’s syndrome
Body Composition
Female
Insulin Resistance
Biomarkers
DOI:
10.1007/s12020-017-1370-x
Publication Date:
2017-07-12T14:59:57Z
AUTHORS (12)
ABSTRACT
Obesity and its metabolic impairments are discussed as major risk factors for sarcopenia leading to sarcopenic obesity. Cushing's syndrome is known to be associated with obesity and muscle atrophy. We compared Cushing's syndrome with matched obese controls regarding body composition, physical performance, and biochemical markers to test the hypothesis that Cushing's syndrome could be a model for sarcopenic obesity.By propensity score matching, 47 controls were selected by body mass index and gender as obese controls. Fat mass and muscle mass were measured by bioelectrical impedance analysis. Muscle function was assessed by chair rising test and hand grip strength. Biochemical markers of glucose and lipid metabolism and inflammation (hsCRP) were measured in peripheral blood.Muscle mass did not differ between Cushing's syndrome and obese controls. However, Cushing's syndrome patients showed significantly greater chair rising time (9.5 s vs. 7.3 s, p = 0.008) and significantly lower hand grip strength (32.1 kg vs. 36.8 kg, p = 0.003). Cushing's syndrome patients with impaired fasting glucose have shown the highest limitations in hand grip strength and chair rising time.Similar to published data in ageing medicine, Cushing's syndrome patients show loss of muscle function that cannot be explained by loss of muscle mass. Impaired muscle quality due to fat infiltration may be the reason. This is supported by the observation that Cushing's syndrome patients with impaired glucose metabolism show strongest deterioration of muscle function. Research in sarcopenic obesity in elderly is hampered by confounding comorbidities and polypharmacy. As Cushing's syndrome patients are frequently free of comorbidities and as Cushing's syndrome is potentially curable we suggest Cushing's syndrome as a clinical model for further research in sarcopenic obesity.
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