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  • Insulin resistance  (2)
  • chronic renal failure  (2)
  • electrolytes  (2)
  • 1
    ISSN: 1432-0428
    Keywords: Insulin resistance ; hyperinsulinaemia ; glucose tolerance ; chronic renal failure ; aerobic work capacity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Tissue sensitivity to insulin and aerobic work capacity was measured in patients with mild to moderate progressive chronic renal failure. Twenty-nine non-diabetic patients with a glomerular filtration rate of 25 ml·min−1·1.73 m−2 (11–43) (median, range) and 15 sex, age, and body mass index matched control subjects with normal renal function were studied. Fasting blood glucose was comparable and in the non-diabetic range in the two groups as was the oral glucose tolerance test. Patients demonstrated hyperinsulinaemia both during fasting (p〈0.01) and during the test (p〈0.02). The tissue sensitivity to insulin, expressed by the amount of glucose infused during the last 60 min of a 120-min hyperinsulinaemia euglycaemic clamp (M-value) and the M/I ratio, was significantly lower in the patients than in the control subjects (M-value 404±118 vs 494±85 mg glucose/kg body weight, p〈0.02) (M/I ratio 1.77±0.71 vs 2.57±0.70 (mg/(kgBW·min) per pmol/l·100, p〈0.001). The maximal aerobic work capacity was significantly lower in the patients than in the control subjects (24±8 vs 32±11 ml O2/(kg body weight·min), p〈0.02) and positively correlated to the M-value and the M/I ratio in both groups. In conclusion, not only patients with end-stage chronic renal failure but also those with mild to moderate progressive chronic renal failure are insulin resistant and hyperinsulinaemic. The tissue sensitivity to insulin is correlated to the maximal aerobic work capacity suggesting that these patients might benefit from physical training programmes.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-0428
    Keywords: Key words Insulin resistance ; hyperinsulinaemia ; glucose tolerance ; chronic renal failure ; aerobic work capacity.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Tissue sensitivity to insulin and aerobic work capacity was measured in patients with mild to moderate progressive chronic renal failure. Twenty-nine non-diabetic patients with a glomerular filtration rate of 25 ml · min−1· 1.73 m−2 (11–43) (median, range) and 15 sex, age, and body mass index matched control subjects with normal renal function were studied. Fasting blood glucose was comparable and in the non-diabetic range in the two groups as was the oral glucose tolerance test. Patients demonstrated hyperinsulinaemia both during fasting (p 〈 0.01) and during the test (p 〈 0.02). The tissue sensitivity to insulin, expressed by the amount of glucose infused during the last 60 min of a 120-min hyperinsulinaemia euglycaemic clamp (M-value) and the M/I ratio, was significantly lower in the patients than in the control subjects (M-value 404 ± 118 vs 494 ± 85 mg glucose/kg body weight, p 〈 0.02) (M/I ratio 1.77 ± 0.71 vs 2.57 ± 0.70 (mg/(kgBW · min) per pmol/l · 100, p 〈 0.001). The maximal aerobic work capacity was significantly lower in the patients than in the control subjects (24 ± 8 vs 32 ± 11 ml O2/(kg body weight · min), p 〈 0.02) and positively correlated to the M-value and the M/I ratio in both groups. In conclusion, not only patients with end-stage chronic renal failure but also those with mild to moderate progressive chronic renal failure are insulin resistant and hyperinsulinaemic. The tissue sensitivity to insulin is correlated to the maximal aerobic work capacity suggesting that these patients might benefit from physical training programmes. [Diabetologia (1995) 38: 565–572]
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1432-0428
    Keywords: Insulin resistance ; Type 2 (non-insulin-dependent) diabetes mellitus ; hyperinsulinaemic clamp ; indirect calorimetry ; forearm glucose uptake ; muscle ; glycogen synthase ; insulin receptor kinase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Insulin resistant glucose metabolism is a key element in the pathogenesis of Type 2 (non-insulin-dependent) diabetes mellitus. Insulin resistance may be of both primary (genetic) and secondary (metabolic) origin. Before and after diet-induced improvement of glycaemic control seven obese patients with newly-diagnosed Type 2 diabetes were studied with the euglycaemic clamp technique in combination with indirect calorimetry and forearm glucose balance. Muscle biopsies were obtained in the basal state and again after 3 h of hyperinsulinaemia (200 mU/l) for studies of insulin receptor and glycogen synthase activities. Similar studies were performed in seven matched control subjects. Insulin-stimulated glucose utilization improved from 110±11 to 183±23 mg·m−2·min−1 (p〈0.03); control subjects: 219+23 mg·m−2·min−1 (p=NS, vs post-diet Type 2 diabetes). Nonoxidative glucose disposal increased from 74±17 to 138+19 mg·m−2·min−1 (p〈0.03), control subjects: 159±22 mg· m−2·m−1 (p=NS, vs post-diet Type 2 diabetic patients). Forearm blood glucose uptake during hyperinsulinaemia increased from 1.58±0.54 to 3.35±0.23 μmol·l−1·min−1 (p〈0.05), control subjects: 2.99±0.86 μmol·l−1·min−1 (p=NS, vs post-diet Type 2 diabetes). After diet therapy the increase in insulin sensitivity correlated with reductions in fasting plasma glucose levels (r=0.97, p〈0.001), reductions in serum fructosamine (r=0.77, p〈0.05), and weight loss (r=0.78, p〈0.05). Values of muscle glycogen synthase sensitivity to glucose 6-phosphate (A0.5 for glucose 6-phosphate) were similar in the basal state. However, insulin stimulation of glycogen synthase was more pronounced after diet treatment (A0.5: 0.43±0.06 (before) vs 0.30±0.04 mmol/l (after); p〈0.03; control subjects: 0.22±0.03 mmol/l). Muscle insulin receptor binding and kinase activity were similar before and after diet treatment and comparable to values in the control group. The data suggest that impaired insulin stimulation of in vivo glucose turn-over and muscle glycogen synthase activity tend to be restored during successful diet treatment of patients with Type 2 diabetes.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1432-0428
    Keywords: Key words Diabetes ; diabetic neuropathy ; electrolytes ; hyperglycaemia ; nerve conduction ; somatostatin.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Insufficient metabolic control in diabetes mellitus is associated with a reversible reduction in nerve conduction velocity, but the mechanism behind this phenomenon is unknown. To examine the effect of acute hyperglycaemia on nerve conduction eight non-diabetic men (20–49 years of age) with no signs of peripheral neuropathy were studied before and after 3 h of hyperglycaemic clamping (plasma glucose ≈ 15 mmol/l), while insulin secretion was suppressed by somatostatin [Study 1]. Nerve conduction velocity, as determined in the proximal part of the median nerve, fell by 2.8 ± 3.0 m/s (2p-value: 0.033). However, during euglycaemic clamping (plasma glucose ≈ 5 mmol/l) in five non-diabetic men (19–38 years of age) infused solely with somatostatin [Study 2], a comparable decrement in nerve conduction velocity was found (1.7 ± 1.3 m/s, 2p-value: 0.043). In both studies relative hypoinsulinaemia was present. Serum-sodium decreased significantly (143 ± 1 mmol/l vs 137 ± 1 mmol/l [Study 1] and 143 ± 1 mmol/l vs 142 ± 2 mmol/l [Study 2]), while serum-potassium increased. In conclusion, the slight but significant reduction in nerve conduction velocity observed in both studies appears to be correlated to electrolyte changes. However, an effect of hypersomatostatinaemia or the hormonal changes associated with this cannot be excluded, while short-term hyperglycaemia per se seems to be without effect on nerve conduction velocity. [Diabetologia (1994) 37: 1216–1220]
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0428
    Keywords: Diabetes ; diabetic neuropathy ; electrolytes ; hyperglycaemia ; nerve conduction ; somatostatin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Insufficient metabolic control in diabetes mellitus is associated with a reversible reduction in nerve conduction velocity, but the mechanism behind this phenomenon is unknown. To examine the effect of acute hyperglycaemia on nerve conduction eight non-diabetic men (20–49 years of age) with no signs of peripheral neuropathy were studied before and after 3 h of hyperglycaemic clamping (plasma glucose ≈ 15 mmol/l), while insulin secretion was suppressed by somatostatin [Study 1]. Nerve conduction velocity, as determined in the proximal part of the median nerve, fell by 2.8±3.0 m/s (2p-value: 0.033). However, during euglycaemic clamping (plasma glucose ≈ 5 mmol/l) in five non-diabetic men (19–38 years of age) infused solely with somatostatin [Study 2], a comparable decrement in nerve conduction velocity was found (1.7±1.3 m/s, 2p-value: 0.043). In both studies relative hypoinsulinaemia was present. Serum-sodium decreased significantly (143±1 mmol/l vs 137±1 mmol/l [Study 1] and 143±1 mmol/l vs 142±2 mmol/l [Study 2]), while serum-potassium increased. In conclusion, the slight but significant reduction in nerve conduction velocity observed in both studies appears to be correlated to electrolyte changes. However, an effect of hypersomatostatinaemia or the hormonal changes associated with this cannot be excluded, while short-term hyperglycaemia per se seems to be without effect on nerve conduction velocity.
    Type of Medium: Electronic Resource
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