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Biomedical subjects

J Skrha

Publications and source records attributed to J Skrha.

At least 73 records · Page 4Linked to original sources
PubMed1998

[The effect of insulin in primary hyperaldosteronism].

BACKGROUND: Deteriorated insulin resistance was described in patients with essential hypertension. The objective of the present study was to test at the receptor and postreceptor level the presence of insulin resistance in hypertension with primary hyperaldosteronism. METHODS AND RESULTS: The diagnosis of primary hyperaldosteronism was assessed by means of biochemical and imaging methods in 123 hypertensive patients with a normal glucose tolerance (mean age 49.8 +/- 12.9 years, range 20-65 years, BMI 28.3 +/- 4.8 kg/m2). The blood pressure was monitored for 24 hours by a Spacelab tonometer (systolic BP 168 +/- 21 mm Hg, diastolic BP 103 +/- 9 mm Hg, plasma aldosterone in a recumbent position 426 +/- 472 pg/ml (normal values under 150 pg/ml), concentration of serum potassium 3.6 +/- 0.6 mmol/l. The control group was formed by seven volunteers matched for age and BMI. The patients had a normal basal blood sugar level in the morning (5.0 +/- 0.6 mmol/l), the basal insulinaemia was 19.5 +/- 10.2 mU/l. The insulin resistance was examined using the method of an euglycaemic hyperinsulinaemic clamp on Biostator at an insulin infusion rate of 1 mU/kg/min. Concurrently insulin receptors on red blood cells were assessed. The plasma potassium concentration was maintained by means of insulin receptors on erythrocytes. The potassium plasma concentration was maintained by means of a linear dosage device with potassium at constant physiological levels (after previous supplementation). In patients with primary hyperaldosteronism the authors observed, as compared with healthy controls, a lower glucose consumption during the clamping (glucose disposal rate 18.7 +/- 4.8 vs 29.3 +/- 3.7 mumol/kg/min, p < 0.01), a rise of the metabolic glucose clearance (3.8 +/- 1.5 vs. 7.0 +/- 1.1 ml/kg/min, p < 0.01 and an index of tissue sensitivity for insulin) 23.7 +/- 9.8 vs. 37.5 +/- 11.6 mumol/kg/min per mU/l x 100, p < 0.02). The characteristics of insulin receptors in patients with primary hyperaldosteronism did not differ from normal values. No correlation was found between the plasma concentration of aldosterone and the index of tissue sensitivity for insulin (r = 0.011, NS). CONCLUSIONS: It may be stated that primary hyperaldosteronism is associated with insulin resistance at the postreceptor level. Its pathogenesis has not been elucidated so far and will be the object of future research.

Adult↗
PubMed1998

The influence of NO synthase inhibitor and free oxygen radicals scavenger--methylene blue--on streptozotocin-induced diabetes in rats.

The excessive production of nitric oxide (NO) and the subsequent increase of local oxidative stress is suggested as one of the pathophysiological mechanisms of streptozotocin-induced diabetes. It was reported that the administration of NO synthase inhibitors partially attenuated the development of streptozotocin-induced diabetes and reduced hyperglycaemia. Here we have studied the influence of methylene blue, which combines the properties of NO synthase inhibitor with antioxidant effects. The experiments were performed on male rats divided into four groups: control, diabetic (single dose of 70 mg of streptozotocin/kg i.p.), methylene blue (50 mg/kg in the food) and diabetic simultaneously fed with methylene blue. After 45 days the experiments were discontinued by decapitation. Serum glycaemia, glycated haemoglobin and oxidative stress parameters (plasma malondialdehyde concentration and erythrocyte superoxide dismutase activity) were significantly higher in the diabetic group. Simultaneous methylene blue administration partially reduced glycaemia and glycated haemoglobin, but did not decrease oxidative stress. We conclude that NO synthase inhibitor methylene blue partially attenuates the development of streptozotocin-induced diabetes in male rats, but does not reduce the development of oxidative stress in the diabetic group.

Animals↗
PubMed1998

Haemostasis, cytoadhesive molecules (sE-selectin and sICAM-1) and inflammatory markers in non-insulin dependent diabetes mellitus (NIDDM).

Non-insulin dependent diabetes mellitus (NIDDM) is connected with a higher incidence of macrovascular atherosclerotic disorders. The aim of the study was to detect any difference in levels of "cardiovascular risk factors"--fibrinogen, PAI-1 and inflammation response (documented by an increase of protein of acute phase orosomucoid) and of soluble cytoadhesive molecule sE-selectin and sICAM-1 (as markers of endothelial dysfunction) in blood plasma of 118 patients with NIDDM in comparison to the levels in blood plasma of 59 healthy persons as a control group. We observed higher levels of fibrinogen (fibrinogen level was 3.44 +/- 1.02 g/l in NIDDM pts versus 2.44 +/- 0.55 g/l in control group, p < 0.01) and PAI-1 Ag concentration was 159.7 +/- 110.3 ng/ml in NIDDM pts versus 51.43 +/- 24.64 ng/ml in control group, p < 0.01) together with an increase of acute phase protein orosomucoid as a "inflammatory response marker" (orosomucoid concentration was 0.85 +/- 0.23 g/l in NIDDM pts versus 0.54 +/- 0.18 g/l in control group, p < 0.01) in patients with NIDDM. The increase of these "cardiovascular risk factors" levels will be probably induced by higher activity of inflammatory cytokines IL-1 beta and/or TNF alpha in NIDDM patients, because both are inducers of orosomucoid fibrinogen and PAI-1 synthesis. This hypothesis is also supported by observation of higher levels of soluble cytoadhesive molecules sE-selectin (sE-selectin level was 64.25 +/- 26.8 ng/ml in NIDDM pts versus 46.64 +/- 29.57 ng/ml in control group, p < 0.01) and sICAM-1 (sICAM-1 level was 307.71 +/- 86.2 ng/ml in NIDDM pts versus 255.6 +/- 58.0 ng/ml in control group, p < 0.01) in patients with NIDDM. Both cytoadhesive molecules are produced by endothelial cells which are influenced by IL-1 beta and/or TNF alpha. According to these findings we suppose that an "inflammation" plays an important role in the evolution of atherosclerotic process at NIDDM together with the known influence of glucose and lipid metabolism pathology.

Cardiovascular Diseases↗
PubMed1998

The effect of glycosaminoglycan sulodexide on oxidative stress and fibrinolysis in diabetes mellitus.

Glycosaminoglycan sulodexide may influence morphology and functional properties of the basement membranes in microvessels. The aim of this study was to evaluate the effect of sulodexide administration on albuminuria and on different biochemical variables indicating endothelial dysfunction, oxidative stress and fibrinolysis in diabetic patients. Twenty diabetic patients of both types with micro- or macroalbuminuria were selected for sulodexide treatment. Daily dose of 600 U (60 mg) was injected intramuscularly five days a week. Fifteen doses were applied during 3 weeks. The patients were examined before and after treatment as well as 6 months later. No changes of diabetes control were observed during the study and after 6 months of wash-out period. Significant decrease of albuminuria (p < 0.001) was observed during the sulodexide administration with the following increase to pretreated values during the wash-out period. A decrease of serum N-acetyl-beta-glucosaminidase (NAG) activity (p < 0.03) at the end of treatment as compared to pretreated values was found in the whole group of diabetic patients. Slight reduction of oxidative stress expressed by malondialdehyde and superoxide dismutase was apparent after treatment but no simultaneous change in fibrinolysis was observed. Sulodexide may have some protective effects influencing functional properties of the basement membrane as manifested by lowered albuminuria. In addition, it may slightly decrease oxidative stress in diabetic patients and it could stabilize endothelial cells.

Acetylglucosaminidase↗
PubMed1998

[Personal experience with the treatment of organic hyperinsulinism].

In 1981-1997 at the Third Medical Clinic 52 patients with confirmed organic hyperinsulinism were treated. Forty-three were operated and the remaining nine were treated conservatively. An insulinoma was removed surgically in 35 patients, in one female microadenomatosis was detected. The operation was successful in 84%, while topographic preoperative examination aroused suspicion of a focus (i.e. insulinoma) only in 49% of the operated patients. A total of 11 patients (four after surgery and seven not operated) were treated successfully with diazoxide, in nine patients this treatment is still administered. According to the response to diazoxide it is possible to differentiate "responsive" and "non-responsive" insulinomas. Pharmacological treatment is thus justified only in the first group of patients. Surgically and pharmacologically treated patients have no signs of hyperinsulinism. The authors experience suggests that surgical treatment is indicated when the diagnosis is unequivocal even when the topographic finding of imaging methods is negative, as in 35% of operated patients the insulinoma was found only on operation.

Adolescent↗
PubMed1997

The effect of fasting and vitamin E on insulin action in obese type 2 diabetes mellitus.

The influence of either short-term fasting or vitamin E administration on insulin action was studied in two groups of obese Type 2 diabetic patients. Twelve patients underwent 7 days of fasting (group A), whereas 600 mg of vitamin E was administered daily during 3 months in 9 diabetic patients (group B). Insulin action was examined by using hyperinsulinemic isoglycemic clamps (insulin infusion rate, 1.0 mU/kg/min) and insulin receptors on erythrocytes before and after respective regimens. An increase of glucose disposal rate (29.5 +/- 8.9 vs. 24.0 +/- 7.5 mumol/kg/min, p < 0.01) and an increase of metabolic clearance rate of glucose (4.0 +/- 2.5 vs. 2.3 +/- 0.9 mL/kg/min, p < 0.01) were observed in group A after fasting. On the contrary, decreases of glucose disposal rate (21.3 +/- 8.5 vs. 26.6 +/- 9.8 mumol/kg/min, p < 0.02), metabolic clearance rate of glucose (2.9 +/- 0.8 vs. 3.7 +/- 1.7 mL/kg/min, p < 0.05), and insulin receptor number (p < 0.01) were found after vitamin E administration as compared with pretreated values. A worsening of diabetes control as observed by an increase of HbA1C (p < 0.01) was present in the latter group. In summary, we found an improvement of insulin action after short-term fasting in contrast with the worsening of metabolic parameters after vitamin E administration in obese Type 2 diabetic patients.

Administration, Oral↗
PubMed1997

[The effect of a short-term reducing diet on the effect of insulin in type 2 diabetes mellitus].

BACKGROUND: Insulin resistance is in addition to impaired beta-cell function decisive for the development of type 2 diabetes. It is also known that obesity creates conditions for the development of insulin resistance. The authors tried therefore to influence insulin sensitivity by short-term reducing diets in obese type 2 diabetics. METHODS AND RESULTS: The group of patients comprised 12 obese type 2 diabetics, BMI: 40.3 +/- 8.9 kg/m2, age 50 +/- 8 years. The control group was formed by 12 healthy non-obese subjects. The following parameters of glucose tolerance were assessed: total glucose consumption to maintain euglycaemia (M) during an isoglycaemic hyperinsulinaemic clamp on a Biostator, index of tissue sensitivity to insulin (M/I), metabolic glucose clearance (MCRG), number of insulin receptors on erythrocytes (Ro) and the insulin affinity for receptors (Ko). A reducing diet, 600 kcal/day, was served for 7 days during hospitalization. The body weight of diabetics dropped by 3.2 +/- 1.5 kg, p < 0.001, there was a significant decline of the basal blood sugar level (G(o)) from 11.4 +/- 3.6 to 8.4 +/- 3.0 mmol/l, p < 0.01; 2 there was a significant reduction of the serum insulin level (Io) from 30 +/- 18 to 27 +/- 19 mU/l, p < 0.02, whereby glucose uptake M increased from 24.0 +/- 7.5 to 29.5 +/- 8.9 mumol/kg/min, p < 0.01 and at the same time the metabolic glucose clearance increased from 2.3 +/- 0.9 to 4.0 +/- 2.5 ml/kg/min, p < 0.01, while the index of tissue sensitivity to insulin M/I increased less significantly from 16.3 +/- 7.4 to 18.0 +/- 10.5 mumol/kg/min per mU x 100). There was a decline in the number of insulin receptors on erythrocytes from 245 +/- 66 to 192 +/- 61 pmol/l, p < 0.02, whereby their affinity improved: 12.8 +/- 3.9 as compared with 17.3 +/- 5.4 10(8) l/mol, p < 0.01 but the insulin bond remained unchanged. CONCLUSIONS: A short-term reducing diet leads to improvement of the majority of investigated indicators which is manifested in particular by improved action of insulin, above all at a postreceptor level. Significant reduction of the number of insulin receptors was partly compensated by improved affinity, while the insulin bond did not change in a marked way.

Blood Glucose↗
PubMed1997

Glycosaminoglycan sulodexide decreases albuminuria in diabetic patients.

Albuminuria is a dominant biochemical feature of developing diabetic nephropathy. A disturbed metabolism of heparan sulphate characterized by an increased loss of anionic charges in the basement membrane has been considered as one of the main factors causing an increased albumin output into urine. All therapeutic approaches inducing a reduction of the albumin excretion rate (AER) have a protective effect on renal function. The effect of glycosaminoglycan sulodexide on albuminuria was studied in a group of 53 diabetic patients (26 Type 1 and 27 Type 2) with micro and macroalbuminuria. Sulodexide (Vessel Due F) was administered intramuscularly in one daily dose (600 lipasemic units) for 3 weeks followed by a 6 week wash-out period. A significant decrease of AER was found in a total cohort of patients following just 1 week of sulodexide treatment (mean 162 micrograms/min, range 10-2708 micrograms/min vs mean 248 micrograms/min, range 20-3160 micrograms/min, P < 0.001). This effect lasted 3-6 weeks after drug withdrawal. Similar results were obtained if Type 1 and Type 2 diabetic patients were evaluated separately but a delay of the AER reduction was observed in the latter group. In all patients the mean AER was reduced to 60-65% of the initial values. A greater effect of sulodexide on albuminuria was observed in patients with AER above 200 micrograms/min than in those with microalbuminuria (a reduction to 47 vs 65% of the initial output). Sulodexide did not significantly reduce albuminuria in 28% of diabetic patients ('non-responders'). In conclusion, glycosaminoglycan sulodexide may reduce AER in patients with micro or macroalbuminuria and it could slow down development of diabetic nephropathy.

Adult↗
PubMed1997

[The effect of sulodexide, a glycosaminoglycan, on albuminuria in diabetic patients].

UNLABELLED: The authors administered to type 1 diabetics (n = 15) or type 2 diabetics (n = 20) with microalbuminuria or macroalbuminuria for a period of 15 days i.m. doses of sulodexide (Vessel Due F), 600 i.u. (i.e. 60 mg). The evaluation of the whole group revealed a statistically significant reduction of the original mean value of albuminuria (509 +/- 127 ug/min) already during the first week of sulodexide administration (382 +/- 105). A further decrease was recorded after the second and third week of treatment (326 +/- 89, 319 +/- 85 ug/min). While in diabetics with microalbuminuria < 100 micrograms/min the mean levels of excreted albumin were not affected, in diabetics with macroalbuminuria 200 ug/min a significant reduction of albuminuria persisted (p < 0.001) achieved during sulodexide treatment persisted for three weeks after completed treatment. No differences were found between the results of type 1 and type 2 diabetics. CONCLUSION: Seventy-seven per cent type 1 and type 2 diabetics responded to parenteral sulodexide administration for 15 days by a statistically significant reduction of albumin.

Adult↗
PubMed1996

[Early diagnosis of impaired glomerular and renal tubule function in patients with acromegaly].

BACKGROUND: Albuminuria (A), increased urinary excretion of glycosaminoglycans (GAG) and increased activity of N-acetyl-beta-glucosaminidase (NAG) in urine are early markers of glomerular and tubular changes in various pathological conditions at a time when renal functions do not yet display impaired function and when the changes are still reversible. The objective of the presented study was to assess to what extent these early changes may play a part in acromegaly. METHODS AND RESULTS: In a group of 24 acromegalic patients and in 18 healthy controls the authors examined the microalbuminuria (RIA Immunotech Prague), urinary excretion of glycosaminoglycans (spectrophotometrically by the carbazole method) and they assessed the NAG activity in urine (spectrophotometrically). In acromegalic patients before surgical and pharmacological treatment the authors found, as compared with healthy controls, increased urinary excretion of GAG [4.4 (0.9-22.7) g/mol creat. vs. 2.1 (0.8-5.5) g/mol creat, p < or = 0.001], elevated albuminuria [3.6 (0.3-37.4) g/mol creat. vs. 0.5 (0.1-2.2) g/mol creat, p < or = 0.001 and an enhanced NAG activity [1005 (345-2935) U/l vs. 470 (195-1135) U/l, p < or = 0.001]. The parameters of albuminuria and urinary GAG excretion characterize rather glomerular renal function, they correlate mutually (r = 0.64 p < or = 0.001), while the urinary NAG activity, depending on tubular function, does not correlate with them. No correlation of these parameters with the IGI concentration (for A: 0.3, for GAG: -0.04 and for NAG: -0.02 according to Pearson was found. CONCLUSIONS: In hormonally active acromegalic patients without apparent altered renal functions (normal serum creatinine, Albustix negative) the authors detected early changes of glomerular and tubular functions. They found a significant correction between albuminuria and GAG excretion.

Acetylglucosaminidase↗
PubMed1996

[Levels of tissue-type plasminogen activator (T-PA), its inhibitor (PAI-1) and fibrinogen in the blood of patients with type 1 and 2 diabetes mellitus].

BACKGROUND: Fibrinogen (Fgb), the tissue activator of plasminogen (t-PA) and its inhibitor (PAI-1) are described as so-called cardiovascular risk factors. The objective of the present investigation was to assess the occurrence of the mentioned risk factors (Fbg, t-PA and PAI-1) in diabetes mellitus (DM) type 1 and 2, compare them with findings in a healthy control group and the two types of diabetes mutually. METHODS AND RESULTS: Fifty patients with type 1 DM were examined (mean BMI 23.8), 59 patients with type 2 DM (mean BMI 28) and 33 healthy subjects as controls (mean BMI 24.6). Both groups of diabetics were compensated. To assess the t-PA and PAI-1 concentration the ELISA test was used, Fbg was assessed by Clauss' method. The euglobulin fibrinolysis time (ECLT) was also examined. In both groups of patients with DM higher concentration of t-PA were found (DM type 7.06 +/- 2.4 ng/ml, p < 0.05, DM type 2 15.15 +/- 6.07 ng/mg, control 4.67 +/- 2.87 ng/ml, p < 0.05). In patients with DM type 1 a higher concentration of t-PA was found in patients with retinopathy (8.2 +/- 1.7 ng/ml than in patients with DM type 1 without retinopathy (6.9 +/- 1.3 ng/ml), p < 0.05). The PA-1 concentration was, as compared with controls, raised only in type 2 diabetics (DM type 2 124.57 +/- 47.22 ng/ml, control 88.57 +/- 15.7 ng/ml p < 0.05). Between the two groups also a difference in the PAI-1 level was found (DM type 179.25 +/- 17.95 ng/ml, vs. DM type 2, p < 0.05). With these findings corresponded the ECLT activation in DM type 1 (203.4 +/- 76.8 min. vs. ECLT in the control group 276.08 +/- 84.87 min., p < 0.05) and conversely a reduction of the euglobulin fibrinolysis in type 2 DM (448 +/- 117 min.), as compared with the controls (p < 0.05), as well as compared with DM type 1 (p < 0.05). The fibrinogen level was also elevated only in DM type 2 (3.619 +/- 0.69 g/l) as compared with the control group (2.42 +/- 0.42 g/l, p < 0.05) as well as compared with DM type 1 (2.53 +/- 0.47 g/l, p < 0.05). No difference was found in the fibrinogen level between DM type 1 and the control group. CONCLUSIONS: In both groups of patients with diabetes mellitus type 1 and 2 among the mentioned cardiovascular risk factors only a raised t-PA concentration was recorded. Concurrent elevation of PAI-1 and fibrinogen was found only in diabetes mellitus type 2.

Adult↗
PubMed1996

Relationship of oxidative stress and fibrinolysis in diabetes mellitus.

This study attempted to verify the existence of a relationship between oxidative stress documented by malondialdehyde (MDA) and superoxide dismutase (SOD) and fibrinolysis analysed by tissue plasminogen activator (tPA) and its inhibitor (PAI-1) in diabetes mellitus. Forty-seven patients with Type 1 (n = 27) and Type 2 (n = 20) diabetes were examined together with 20 non-diabetic controls. The following were analysed: plasma MDA concentration, SOD activity in erythrocytes, tPA activity and antigen, PAI-1 activity and antigen, fasting blood glucose, fructosamine, glycated haemoglobin (HbAlc), and urine albumin. SOD activity was decreased in patients with diabetes. This contrasted with an increased plasma MDA concentration especially in Type 2 diabetes as compared with Type 1 or healthy persons (p < 0.001). tPA activity was increased in both groups of patients with diabetes as compared to healthy persons (p < 0.001), PAI-1 activity was higher in Type 2 diabetes with vascular changes than in the remaining subgroups (p < 0.001). Multivariate analysis revealed a significant positive relationship between plasma MDA concentrations and PAI-1 antigen (r = 0.53, p < 0.001) and a negative relationship between SOD and tPA activities (r = -0.53, p < 0.01). We conclude that oxidative stress may modulate fibrinolytic properties in diabetes mellitus.

Adult↗
PubMed1996

Comparison of insulin sensitivity in patients with insulinoma and obese Type 2 diabetes mellitus.

Insulin sensitivity was evaluated in 16 insulinoma patients and in 15 obese persons with Type 2 diabetes mellitus by using hyperinsulinaemic clamps and analysis of insulin receptor characteristics on erythrocytes. Significantly decreased insulin sensitivity index (M/l) was found in both insulinoma and obese Type 2 diabetic patients as compared with healthy non-obese controls (21.2 +/- 2.2 and 19.5 +/- 2.6 vs 40.3 +/- 3.7 mumol.kg-1.min-1 per mU.l-1 x 100, p < 0.001). No difference was observed between both groups of patients. Metabolic clearance rate of glucose was strongly reduced in obese diabetic patients but it was normal in insulinoma patients in comparison with healthy persons (2.7 +/- 0.4 vs 8.7 +/- 0.6 or 7.9 +/- 0.7 ml.kg-1.min-1, p < 0.001). A decreased insulin binding on specific receptors caused by reduced binding capacity was observed only in insulinoma patients but not in obese Type 2 diabetic patients. A significant negative correlation was proved between body mass index (BMI) and insulin sensitivity index (r = -0.82, p < 0.001) indicating that BMI is the main determining factor of insulin resistance in the total cohort of examined patients. We conclude that insulin resistance was caused by postreceptor changes in obese Type 2 diabetes, whereas a decreased insulin binding capacity together with post-receptor defect was present in insulinoma patients.

Adult↗
PubMed1996

[Levels of lactic acid in type II diabetics treated with buformin].

The objective of the work was to assess the blood lactate levels in type 2 diabetics selected at random, treated for prolonged periods with buformin. 77% of the investigated group of diabetics (N = 70) had elevated blood lactate levels and 16% of them had hyperlactataemia (more than 5.0 mmol/l). In 33% patients with an originally elevated lactataemia after 12 weeks of discontinued buformin treatment the lactic acid blood levels reached normal values. The lactate levels declined significantly (by more than 25% of the original value) after 6 weeks without buformin treatment in another 45% of the diabetic patients. In 18% of the investigated patients, who had high lactate levels even after discontinuation of treatment, in two-thirds neither impaired function of the kidneys and liver nor cardiac disease or alcoholism were detected.

Adult↗
PubMed1996

[Personal experience with the diagnosis of organic hyperinsulinism].

The diagnosis of organic hyperinsulinism was established in 47 patients based on the typical clinical symptomatology supported by laboratory evidence of hypoglycaemia and raised serum insulin concentrations. For the diagnosis of the disease the test of controlled fasting is suited best. During this test and after its termination the blood sugar level (in mmol/l), serum insulin (in mU/l) and their ratio (insulin/blood sugar) are assessed. In all patients the test had to be discontinued because clinical manifestations of hypoglycaemia developed which are typical for organic hyperinsulinism. Other methods, incl, examination by means of an isoglycemic clamp or insulin receptors are not specific and cannot be used for diagnosis. As to imaging (localisation) methods in the examined group the lowest yield was obtained by computed tomography (positive only in one patient), better results were obtained by sonography (21%) and angiography resp, (45%). When methods were combined an insulinoma was detected in 55% patients while on operation it was found in 82% patients. The authors' experience provides evidence that for the diagnosis of organic hyperinsulinism a decisive role is played by the clinical symptomatology supplemented by laboratory evidence of hypoglycaemia and possibly by a raised serum insulin concentration.

Adolescent↗
PubMed1995

[Insulin resistance and hyperlipoproteinemia].

Insulin resistance is part of the so-called plurimetabolic syndrome where it was observed in association with various signs among which the association with impaired serum lipids is very frequent. The most frequent deviations are hypertriacylglycerolaemia (in particular VLDL), low HDL-cholesterol and elevated serum levels of non-esterified fatty acids. Some hitherto assembled findings suggest a close relationship between glucose and lipid metabolism. Enhanced oxidation of non-esterified fatty acids leads to inhibition of glucose oxidation and this may participate in the development of insulin resistance. Changes in cholesterol and triacylglycerol levels seem to be rather the consequence than cause of the development of insulin resistance. It cannot be ruled out that insulin resistance is genetically conditioned and this would explain the other associated changes as secondary ones.

Glucose↗