|Year : 2014 | Volume
| Issue : 1 | Page : 40-43
Insulin sensitivity and skeletal muscle function in adult men with type II diabetes mellitus
Department of Physiology, Sapthagiri Institute of Medical Sciences, Bengaluru, Karnataka, India
|Date of Web Publication||15-Apr-2014|
Department of Physiology, Sapthagiri Institute of Medical Sciences, Hesaraghatta Main Road, Bengaluru, Karnataka
Source of Support: None, Conflict of Interest: None
Background: Insulin resistance (IR) is an important component in the pathogenesis of type II diabetes. As skeletal muscle is known to be the key site for glucose disposal, any physiological or structural alterations might lead to IR. Aim: Assessment of insulin sensitivity and skeletal muscle function in diabetic men. Materials and Methods: A total of 30 diabetic men were matched with 30 controls. Static and dynamic endurance for muscle function and insulin sensitivity was calculated by homeostatic model assessment. Results: Diabetic men showed early onset of fatigue (P < 0.05) and faster decline of muscle strength for static endurance (P < 0.05) even though muscle mass (MM) was comparable to controls. They had a decreased beta cell function, increased IR and decreased sensitivity. Conclusions: As the diabetic men are prone for skeletal muscle dysfunction, they have to adopt preventive strategies including resistance-training exercise program to improve skeletal muscle function. Skeletal muscle being one of the key sites for glucose disposal, improving the skeletal muscle function will in turn help in improving the insulin sensitivity.
Keywords: Diabetes, insulin sensitivity, skeletal muscle function
|How to cite this article:|
Roopashree N. Insulin sensitivity and skeletal muscle function in adult men with type II diabetes mellitus. Int J Health Allied Sci 2014;3:40-3
|How to cite this URL:|
Roopashree N. Insulin sensitivity and skeletal muscle function in adult men with type II diabetes mellitus. Int J Health Allied Sci [serial online] 2014 [cited 2021 Jan 21];3:40-3. Available from: https://www.ijhas.in/text.asp?2014/3/1/40/130611
| Introduction|| |
There are currently approximately 33 million diabetics in India and this number is expected to rise to about 57 million by year 2025.  Insulin resistance (IR) is an important component in the pathogenesis of type II diabetes due to an impaired biological response to the action of insulin. There are considerable epidemiological data from migrant Indians suggesting less insulin sensitivity in Indians than other ethnic groups. , It is possible that body compositional factors other than the total body fat might predispose to the lowering of the insulin sensitivity.  Skeletal muscle is known to be the key site for glucose disposal. Any physiological and structural alterations might lead to IR. Resistance to insulin-mediated glucose uptake in skeletal muscle is usually associated with obesity and physical inactivity.  This might be due to a loss of insulin-mediated anabolic effects, increased catabolic effects and a reduced ability to clear damaged tissue, all of which will significantly contribute to sarcopenia.  This in turn might lead to analogous changes in the mass and function in the muscle. This study therefore is designed to assess the insulin sensitivity and skeletal muscle function in type II diabetic men of Indian origin with age and gender matched controls.
| Materials and Methods|| |
A hospital based cross-sectional study.
Institutional Ethical Committee approval was obtained for the study. The study population consisted of diabetic patients (disease duration 5-15 years; n = 30) recruited at Endocrinology Out-patient Department, St. John's Medical College Hospital, Bangalore. Age and gender matched healthy controls (n = 30) were recruited in and around the vicinity of St. John's Medical College. Prior to the recruitment, details of the procedures were discussed with the subjects and written informed consent was obtained. A minimum sample size of 30 in each group was required to estimate differences of approximate 10% between control and diabetic patients with power of 0.8 and alpha error at 0.05.
All subjects underwent muscle function assessment (static and dynamic endurance) and insulin sensitivity which was determined by homeostasis model assessment (HOMA).
Inclusion criteria for diabetic group included patients with type II diabetes fulfilling World Health Organization criteria (fasting plasma glucose 40 ≥126 mg/dl or 2-h plasma glucose ≥200 mg/dl) and with duration of diabetes of 5-15 years. The control group included healthy patients with a stable weight over last 2 months. Subjects with active tuberculosis, asthma, cardiovascular disease, history of alcohol intake or hypoglycemic episodes 24 h prior to testing were excluded from the study.
Fasting blood glucose, glycosylated hemoglobin, total cholesterol, lipid profile, 24 h urine protein, and serum insulin levels was estimated in all subjects.
MM was evaluated by the formula MM = (height cm) 2 × (0.0029 × corrected arm muscle area [CAMA]), where CAMA was obtained by the formula [(mid-arm circumference in cm) - (π × triceps skin fold in cm) 2/4 × π] - 10.
Muscle function was evaluated by a load cell (Model TR 12, IPA, Bangalore, India), which measured the strength of the non-dominant forearm flexors and whose signal output was stored in a computer for analysis. First, maximal voluntary contraction (MVC) was recorded 3 times, with constant encouragement, with an interval of at least 1 min between each measurement, and the best of the values used in the analysis. The MVC was corrected for forearm size (standardized MVC[SMVC]) by dividing it by forearm muscle area. The rate of decline of the sustained MVC was also recorded, up to the point when the subject reached 50% of the starting value and this rate (kg/s) was taken as an index of static endurance. Subjects were also asked to repeatedly contract their forearm flexors at a rate of once every 2 s starting at their maximal contraction. The rate of decline to 50% of this stating value was taken as an index of dynamic endurance. In both instances in which endurance was measured, the rate of decline was calculated by fitting biexponential equations (to provide best fit) to the data. In the repeated contractions study (dynamic endurance), running means was used to smooth the data before applying the biexponential curve fit. The different muscle function tests were performed in random order, but adequate rest was given between the tests.
Measurement of insulin sensitivity
FPG (mmol/L) and fasting plasma insulin (FPI, mU/L) concentrations were obtained from all the patients. Insulin sensitivity was estimated using the HOMA.
The HOMA calculator uses the HOMA2 which is an improvised computer model to estimate beta cell function (%B), IR and insulin sensitivity (%S) in all the subjects, from simultaneously measured fasting plasma glucose and FPI values. The estimation of insulin values were obtained using radio immune assay.
Data was checked for normality and was observed that the data is normally distributed. Comparison between the diabetic and control groups was performed using Independent 't' test. Strength of association between various parameters of muscle function and insulin sensitivity was checked using Pearson's correlation coefficient. P < 0.05 was accepted as statistically significant.
| Results|| |
The subject characteristics at baseline are shown in [Table 1]. The diabetic and control groups did not differ by age, height, weight, body mass index, percentage fat, waist hip ratio blood pressure and heart rate.
The basal glucose, glycosylated hemoglobin were significantly higher (P < 0.05) in diabetic group compared with the control group [Table 2]. The beta cell function derived from the HOMA model (HOMA2-%B) was observed to be significantly reduced (P < 0.05) among the diabetic group compared to the control group. The insulin sensitivity (HOMA2-%S) and IR (HOMA2-IR) derived from HOMA model, demonstrated a decrease in sensitivity and an increased resistance in the diabetic group though not statistically significant [Table 2]. Even though, the FPI levels were higher in diabetic groups, there was no statistical significance.
|Table 2: Comparison of biochemical and HOMA derived parameters of study population |
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MM, mean MVC and SMVC were comparable in both the groups. Assessment of skeletal muscle function demonstrates that the onset of fatigue for static endurance (time of onset of fatigue in isometric exercise) was significantly earlier in the diabetics than the controls (P < 0.05). In contrast, rate of decline of strength (RDS) for static endurance in diabetics was significantly faster compared to the controls (P < 0.05). The other muscle parameters like MM, mean MVC, SMVC, time of onset of fatigue and RDS for dynamic endurance was not statistically different between the diabetic and control groups [Table 3].
|Table 3: Comparison of skeletal muscle function parameters in diabetics and controls |
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The muscle function variables namely, the RDS for static endurance [Figure 1], time of onset of fatigue [Figure 2] and RDS for dynamic endurance [Figure 3] showed a negative association with insulin sensitivity. However, the correlation was not statistically significant.
|Figure 1: Relationship of insulin sensitivity and rate of decline of strength (kg/s) for static endurance|
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|Figure 2: Relationship of insulin sensitivity and time of onset of fatigue (in s) for dynamic endurance|
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|Figure 3: Relationship of insulin sensitivity and rate of decline of strength (kg/s) for dynamic endurance|
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| Discussion|| |
Muscle is the major target for insulin-stimulated glucose uptake, the key determinant of total body insulin sensitivity.  Skeletal muscle is known to be resistant to the action of insulin via post-insulin receptor binding defects. Glucose uptake into the muscle cell requires insulin binding into the cell surface receptors and activation of the insulin activating cascade, which in turn facilitates the movement of the glucose across the cell membrane; ultimately glucose is stored as a glycogen or used up as an energy source. 
In our study, diabetic subjects demonstrated a decreased endurance for isometric exercise (static endurance). The rate of onset of fatigue was also faster in diabetic group for isometric exercise. These findings were observed irrespective of the fact that the diabetics and non-diabetics had similar MM and MVC. The diabetic group showed decreased beta cell function, increased IR and decreased insulin sensitivity which can be considered as early warning predictors of onset of type to diabetes. Insulin sensitivity in our subjects was estimated using HOMA. HOMA is shown to be a good surrogate marker for insulin sensitivity which is validated against clamp insulin sensitivity. 
Two recent studies have also shown that muscle strength was significantly lower in subjects with type II diabetes.  It is also reported that resistance to insulin-mediated glucose uptake in skeletal muscle is associated with obesity and physical inactivity.  Further, it has been suggested that there is an association between physical inactivity and reduced insulin sensitivity. Since muscle is a major site of glucose disposal, it is conceivable that the reduced anabolic effect of insulin leads to reduced physical activity and reduced insulin sensitivity.
Park et al. have demonstrated that muscle quality was consistently lower in older adults with type II diabetes. They reasoned that alterations of muscle composition with increase fat infiltration and neuropathic processes involving motor neurons in diabetics may result in poor muscle quality.  A greater and selective atrophy of type IIb fibers has been observed in diabetic animal muscles which may contribute to decline in the strength. 
This study might have important public health implications in India. Adults with diabetes are at increased risk of developing physical disability. Early detection of altered beta cell function along or increased IR and decreased sensitivity in adults can help to initiate potential preventive strategies like resistive-training exercise programs to improve skeletal muscle function in subjects with diabetes. 
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[Figure 1], [Figure 2], [Figure 3]
[Table 1], [Table 2], [Table 3]