Manifest Diabetes Mellitus Research Articles

Роль самоконтроля гликемии в управлении гестационным сахарным диабетом

Gestational diabetes mellitus (GDM) is a disorder characterized by hyperglycemia first recognized during pregnancy that does not meet the criteria of manifest diabetes mellitus (DM). The GDM decompensation can be a common cause of perinatal mortality. GDM is associated with higher rates of preeclampsia and eclampsia, which require emergency caesarean section [1]. Contemporary approach to GDM management includes the need for mandatory self-monitoring of blood glucose. The target blood glucose range cannot be achieved without self-monitoring of blood glucose done by the pregnant woman at home. Glycemic control during pregnancy should be accurate, simple and user-friendly, allowing the pregnant woman to adjust insulin therapy for GDM by herself. Choosing a blood glucose meter is one of the major aspects of blood glucose self-monitoring. From the physician's perspective, compliance with accuracy standards is the most important criterion for blood glucose meter selection, while from the patient’s perspective, the most important criteria are user friendliness, and simplicity of use. Blood glucose level measurement accuracy is improved, and self-monitoring of blood glucose becomes easier due to technical improvements, which results in improved adherence to treatment and higher therapy efficacy. Achieving and maintaining glycemic targets are impossible without active and meaningful participation of the patient with GDM, as well as without self-monitoring of blood glucose with precise and user-friendly blood glucose meter, such as Contour Plus One.

Cardiovascular and metabolic morbidity in women with previous gestational diabetes mellitus: a nationwide register-based cohort study

BackgroundGestational diabetes mellitus (GDM) is associated with adverse pregnancy outcomes and has maternal health implications reaching beyond the perinatal period. We aimed to investigate the incidence and severity of cardiovascular and metabolic morbidity in women with previous GDM in a Danish population and to study whether proxies of impaired beta cell function—insulin treatment during GDM pregnancy and development of subsequent manifest diabetes mellitus—influence incident risk of cardiovascular and metabolic morbidity.MethodsA nationwide register-based cohort study was conducted on the complete cohort of 700,648 women delivering in Denmark during 1997–2018. The exposure variable was GDM and primary outcome was overall cardiovascular and metabolic morbidity. Secondary outcomes were major cardiovascular disease (ischemic heart disease, heart failure, and/or stroke/transient cerebral ischemia), hypertension, dyslipidemia, and venous thrombosis. Severity of morbidity was assessed using number of hospital contacts with diagnosis codes related to cardiovascular and metabolic morbidity and number of redemptions of prescribed medication related to cardiovascular and metabolic morbidity in women who developed cardiovascular and metabolic morbidity after pregnancy.ResultsThe median follow-up period was 10.2–11.9 years with a total range of 0–21.9 years. GDM was associated with increased risk of any cardiovascular and metabolic morbidity (adjusted HR 2.13 [95% CI 2.07–2.20]), major cardiovascular disease (adjusted HR 1.69 [95% CI 1.55–1.84]), hypertension (adjusted HR 1.89 [95% CI 1.82–1.96], dyslipidemia (adjusted HR 4.48 [95% CI 4.28–4.69]), and venous thrombosis (adjusted HR 1.32 [95% CI 1.16–1.50]). Insulin treatment during pregnancy and subsequent development of manifest diabetes exacerbated the risk estimates. Previous GDM was associated with more hospital contacts and more redeemed prescriptions in women developing cardiovascular and metabolic morbidity (p < 0.001).ConclusionsPrevious GDM was associated with significantly higher risk of cardiovascular and metabolic morbidity, especially incident dyslipidemia. Risks were exacerbated by proxies of beta cell impairment. Severity of morbidity was significantly worse if GDM preceded cardiovascular and metabolic morbidity.

The effect of increase in blood glucose level on hearing loss

ObjectivePrevious studies have shown that hearing function is also vulnerable to the effects of diabetes mellitus which can be shown by brainstem auditory evoked potential and distortion product otoacoustic emission recordings. This study aimed to investigate the changes of brainstem auditory evoked potential and distortion product otoacoustic emission in hyperglycemia and whether there is a relationship between reactive oxygen substances production and hearing deterioration in the rat model. Methods25 streptozotocin induced diabetic rats were divided into three groups: control, high blood glucose, and diabetes mellitus. Brainstem auditory evoked potential and distortion product otoacoustic emission were recorded, and thiobarbituric acid reactive substances levels were measured in the brainstem tissue. ResultsAt 8 kHz, the latencies of I, II, III, IV, and V brainstem auditory evoked potential waves in high blood glucose and diabetes mellitus groups were elongated, at 16 kHz, only these wave latencies of the diabetes mellitus group were prolonged compared with the control group. A significant decrease was also found in distortion product otoacoustic emission amplitudes at 4, 6, 8, and 10 kHz in the high blood glucose and diabetes mellitus groups compared to the control group. There was a significant increase in thiobarbituric acid reactive substances values due to the increase in blood glucose levels in the high blood glucose and diabetes mellitus groups compared to the control group. ConclusionThese results suggested that high blood glucose levels may cause hearing impairment not only in the diabetic state but also in the period of hyperglycemia before the onset of manifest diabetes mellitus and reactive oxygen substances may play an important role in the pathophysiology of diabetes mellitus. We suggest that regulating high glucose levels even before the onset of manifest diabetes mellitus may prevent hazardous effects on hearing function. Level of evidenceLevel 3.

METABOLIC CHANGES / INSULIN RESISTANCE IN TUBERCULOSIS PATIENTS: CAUSE OR EFFECT: review

This review article contains current scientific literature data about the impact of infectious diseases and tuberculosis particulary on the formation of systemic insulin resistance in patients. A number of immune reactions have been reported in the host body in response to tuberculosis infection, which may lead to the development of hyperglycemia in TB patients. Some authors believe that such disorders are transient and disappear after a course of specific treatment, others - are inclined to believe that tuberculosis can cause diabetes in people who have not previously suffered from it, and long-term impairment of carbohydrate metabolism that occurs under the time of active tuberculosis process forms a vicious circle in which insufficiently controlled blood glucose levels can lead to aggravated TB and provoke complications in the form of cardiovascular disorders. Also, we found data on the transformation of latent disorders of carbohydrate metabolism in manifest diabetes mellitus during 1-4 years of follow-up of patients with tuberculosis.

Clinical features of the course of overt diabetes mellitus during pregnancy

Objective: to analyze the features of diagnosis, course and outcomes of pregnancy in women with manifest diabetes mellitus.Materials and methods: the study included 19 delivery medical records of women with MDM (manifest diabetes mellitus during pregnancy) and 500 records of women with GDM (gestational diabetes mellitus).Results: Th irteen women out of nineteen were diagnosed with MDM in the fi rst half of pregnancy. Th e average level of glycemia at the onset of the disease was 9,3±3,0 mmol/l. Mean HbA1c was 7,2±1,1%, which signifi cantly exceeded this indicator in GDM. All women with MDM required insulin therapy, while in the group of women with GDM insulin therapy was used in 27.8% of cases. MDM women showed increased rates of preeclampsia (36,8%) compared to GDM women (15%). Fetal macrosomia was more common in MDM women (36.8%) than in GDM women (17%).Conclusion: Th e high frequency of obstetric and perinatal complications of MDM during pregnancy requires the early detection of hyperglycemia and the prompt initiation of insulin therapy. Screening for carbohydrate metabolism disorders at the fi rst prenatal visit and early initiation of insulin therapy reduce maternal and perinatal mortality.

Таурин та його секрети в експериментальній гепатології

Таурин є унікальною амінокислотою. Він має різноманітні біологічні ефекти, спрямовані на підтримку фізіологічного гомеостазу, включаючи антиоксидацію, модуляцію іонного транспорту, осморегуляцію, регуляцію нейротрансмітерів і кон’югацію жовчних кислот. Саме із стабілізуючою дією таурину на мембрани пов’язують його регулюючий вплив на нормалізацію білкового, вуглеводного, електролітного обміну, активність ряду ферментів і гормонів, енергетичні та відновлювальні процеси в організмі, зміцнення імунної системи. Його кон’югування з жовчними кислотами сприяє колоїдній стабільності жовчі, що вкрай необхідно для підтримки нормального рівня холестерину в крові. З нормалізацією обміну таурину в печінці пов’язують лікування і профілактику різних захворювань серцево-судинної системи, печінки, ожиріння, дисліпідемії та атеросклерозу, а також інсулінорезистентності і цукрового діабету, очних хвороб, неврозів і депресій. Метою даної статті є привернення уваги до таурину як до потужного гепатопротектора, ґрунтуючись на експериментальних дослідженнях.

Diabetes and Oral Health: Summary of Current Scientific Evidence for Why Transdisciplinary Collaboration Is Needed

This Perspective provides a brief summary of the scientific evidence for the often two-way links between hyperglycemia, including manifest diabetes mellitus (DM), and oral health. It delivers in a nutshell examples of current scientific evidence for the following oral manifestations of hyperglycemia, along with any available evidence for effect in the opposite direction: periodontal diseases, caries/periapical periodontitis, tooth loss, peri-implantitis, dry mouth (xerostomia/hyposalivation), dysbiosis in the oral microbiome, candidiasis, taste disturbances, burning mouth syndrome, cancer, traumatic ulcers, infections of oral wounds, delayed wound healing, melanin pigmentation, fissured tongue, benign migratory glossitis (geographic tongue), temporomandibular disorders, and osteonecrosis of the jaw. Evidence for effects on quality of life will also be reported. This condensed overview delivers the rationale and sets the stage for the urgent need for delivery of oral and general health care in patient-centered transdisciplinary collaboration for early detection and management of both hyperglycemia and oral diseases to improve quality of life.

Glucose variability in pregnant women with newly diagnosed hyperglycemia

Background: High-performance parallel next-generation sequencing (NGS) allows for identification of various maturity-onset diabetes of the young (MODY) subtypes also during pregnancy. As this method is expensive and time-consuming, it has proposed to use various predictors for the diagnosis of mutation in the hexokinase (GCK)/MODY2 gene, helping to select the patients for subsequent molecular genetic testing. Hyperglycemia due to MODY2 is commonly newly diagnosed during pregnancy; therefore, there is a search for factors specific to this mutation in pregnant women.Aim: To evaluate blood glucose variability in pregnant women with newly diagnosed hyperglycemia at early gestation and to determine the threshold value of the glycemic variability coefficient for pregnant women with a mutation in the GCK/MODY2 gene.Materials and methods: This observational single center study included 41 pregnant women with newly diagnosed early hyperglycemia (not meeting the criteria for manifest diabetes mellitus). Molecular genetic testing was performed in all of them. According to its results, they were retrospectively categorized into two groups: with early gestational diabetes mellitus (GDM, no mutations) and with hyperglycemia related to a mutation in the GCK/MODY2 gene. A comparative analysis of glycemic variability in the two groups was performed. Sensitivity and specificity of the cutoff value for the coefficient of variability as a diagnostic marker of MODY2 were also calculated.Results: The pregnant women with GDM had significantly higher age and body mass index (BMI) than those with MODY2 (p&lt;0.05). There were significant differences in venous fasting plasma glucose and glycated hemoglobin, with these parameters being higher in the pregnant women with MODY2 (p&lt;0.05). In the patients with a mutation in the GCK gene, hyperglycemia was diagnosed earlier and insulin therapy was started earlier during pregnancy than in those with GDM (p&lt;0.05). The ROC analysis of the diagnostic accuracy of the variability coefficient showed that at the threshold CV (coefficient of variation) value of 20.8, the area under the curve was 0.742 (95% confidence intervals 0.597 to 0.888; p&lt;0.005), with the sensitivity of 65% and the specificity of 65.4%.Conclusion: The calculated sensitivity of 65% and specificity of 65.4% for the CV of 20.8 do not allow for its use as an independent selection criterion for subsequent confirmation of MODY2. However, its combination with the A.J. Chakera criteria (BMI&lt;25 kg/m2 and fasting glucose≥5.5 mmol with 68% sensitivity and 96% specificity) allows to clarify the category of pregnant women with newly detected early hyperglycemia, to whom the search for mutations in the GCK gene should be recommended.

Manifest diabetes after gestational diabetes: a double-cohort, long-term follow-up in a Danish population.

The aim was to follow-up two cohorts of women with GDM to investigate the incidence and time of diagnosis of manifest diabetes mellitus (DM) postpartum and identify the risk factors for diabetes in our population. A follow-up study on two independent cohorts having oral glucose tolerance test (OGTT) in 1991/1992 and 2011-2016: Cohort 1 consisted of 406 women including 54 with GDM and 352 with a non-GDM OGTT-test and cohort 2 had 433 women diagnosed with GDM. The first cohort had nearly 25years of follow-up and gave information on magnitude, conversion rate and type of diabetes manifestation. The second cohort was started recently to evaluate whether newer diagnostic criteria and baseline information on the old cohort are still valid for prediction of diabetes risk. The risk of manifest diabetes in cohort 1 at the end of follow-up was six times higher in women with previous GDM compared with non-GDM (RR = 6; 95% CI 4-11). We observed a 70% diabetes rate 25years after pregnancy. Only family history of diabetes in cohort 2 was associated with conversion to manifest diabetes (p = 0.002), also after adjustment for age, BMI, non-Danish origin and smoking during pregnancy (p < 0.001) CONCLUSION: The incidence of diabetes after GDM is higher than that previously reported in Scandinavian populations and the rate of manifest diabetes rises steeply 15years after pregnancy and after 40years of age. The women of cohort 2 with recent GDM are at risk of DM at a higher rate. On this background our results are useful in identifying the time where GDM women may benefit from the effective implementation of evidence-based treatment to postpone and advert manifest DM.

SEVERE METABOLIC SYNDROME AND PRIMARY AMENORRHEA AS MAIN PATHOPHYSIOLOGICAL FEATURES IN A SUBTYPE OF TURNER SYNDROME (46, X, DEL (X) Q 21)

Turner syndrome can be manifest with a considerable genetic and phenotypic variability. This merely accounts for about 50% of patients who do not have the "classic" 45 X genotype. We report the case of a 42-year-old female patient with a 46, X, del (X) q 21 genotype (deletion on the second X chromosome on the long arm). As the patient displayed a non-typical phenotype and was infertile, a diagnosis was established at the age of 24 with no follow-up treatment. As part of our therapy of the individual due to newly manifested diabetes mellitus, our diagnostic workup revealed a severe metabolic syndrome encompassing fatty liver disease, obstructive sleep apnea syndrome and hyperuricemia. Our observations should sensitize physicians treating female patients for one or more aspects of the metabolic syndrome and its presence in Turner syndrome. These patients have an unfavorable cardiovascular profile, in part due to the metabolic syndrome, but also due to factors intrinsic to Turner syndrome.

Gestational diabetes: Glycaemic predictors for fetal macrosomia and maternal risk of future diabetes

AimsTo investigate how glucose levels at diagnosis of gestational diabetes (GDM) are associated with infant birth weight and long-term risk of manifest diabetes mellitus in the mother. MethodsIn a case control study GDM pregnancies (n=2085) were compared with non-GDM pregnancies matched for day of delivery and obstetric unit (n=3792). GDM was defined as capillary blood glucose (cB-glucose) ≥9.0mmol/l (plasma glucose ≥10.0mmol/l) after a 75g oral glucose tolerance test (OGTT). The GDM cohort were followed up 8.5–13.5yrs after initial diagnosis with a questionnaire, answered by 1324 GDM women (65%). ResultsGDM women had higher mean infant birth-weight compared with controls (3682g vs. 3541g, P<0.001). In multiple linear regression analysis, birth weight was positively correlated to fasting cB-glucose at GDM diagnosis (P<0.001), increased week of gestation (P<0.001) and BMI before pregnancy (P<0.003), while 2h OGTT cB-glucose values ≥9.0mmol/l were not related. Infants born to mothers with fasting cB-glucose ≤4.5mmol/l had no increased mean birth-weight or macrosomia (≥4500g) compared to controls. In the follow up 334/1324 women (25%) of the GDM women had developed diabetes, 215 type 2 diabetes, 46 type 1 diabetes and 72 unclassified diabetes. In logistic regression fasting cB-glucose and 2h OGTT cB-glucose at diagnosis of GDM as well as BMI >25 and origin outside Europe were risk factors for manifest diabetes. ConclusionsFasting blood glucose at diagnosis of GDM gives important information besides 2h OGTT glucose about pregnancy outcome and future risk for maternal diabetes.

Diabetes and the breast

Diabetes and the breast

Chapter 1 - Epidemiology of polyneuropathy in diabetes and prediabetes

Diabetic distal symmetric sensorimotor polyneuropathy (DSPN) represents a major health problem, associated with excruciating neuropathic pain, increased morbidity and impaired quality of life. The understanding of its epidemiology is difficult due to methodological issues. Inconsistency in the selection of diagnostic procedures renders comparison between studies problematic. Further problems arise from selection bias due to the inclusion of hospital-based populations. DSPN affects approximately 30% of hospital-based populations, 20% of community-based samples, and 10% of the diabetic population identified by screening. Chronic painful DSPN is present in 13-26% of diabetic patients. Between 25% and 62% of patients with idiopathic peripheral neuropathy have prediabetes. Among pre-diabetic subjects, 11-25% exhibit peripheral neuropathy and 13-26% neuropathic pain. Evidence from population-based studies indicates that there is a gradient in the prevalence of neuropathy. Indeed, the highest frequency is found in patients with manifest diabetes mellitus, followed by individuals with impaired glucose tolerance, then impaired fasting glucose and, finally, those with normoglycemia. The most important etiologic factors are poor glycemic control, age, diabetes duration, visceral obesity, height, hypertension, age, smoking, hypoinsulinemia, and dyslipidemia. Clinic-based data suggest that DSPN is associated with increased mortality in diabetes, but confirmatory prospective population-based studies are required.

Prognostic association of HbA1c and fasting plasma glucose with reduced kidney function in subjects with and without diabetes mellitus. Results from a population-based cohort study from Germany

ObjectiveTo determine the risk for incident reduced kidney function (RKF) of subjects with pre-diabetes (impaired fasting glucose (IFG, 5.6–6.9mmol/L)) or HbA1c-defined pre-diabetes (5.7%–6.4%) and to determine dose–response relationships of fasting glucose and HbA1c with RKF in subjects with manifest diabetes mellitus. MethodIn a German population-based cohort, recruited 2000–2002 with ages 50–74years, log-binomial regression was used to estimate relative risks (RR) with 95% confidence intervals (95%CI) and restricted cubic splines to plot dose–response relationships. ResultsDuring 8years of follow-up, 678 of 3538 study participants developed primary RKF. Although RKF risk factor prevalences and RKF incidences were higher in subjects with pre-diabetes than in subjects with normal FPG and/or HbA1c levels, an increased risk did not persist after adjusting for established cardiovascular risk factors (RR(IFG): 0.97 (95% CI: 0.75–1.25) and RR(HbA1c-defined pre-diabetes): 1.03 (95% CI: 0.86–1.23)). In subjects with manifest diabetes, RKF risk increased linearly to a more than three-fold risk with increasing fasting glucose and HbA1c levels (at HbA1c>6.4%). ConclusionThis study provides further evidence that pre-diabetes may not directly contribute to the development of kidney disease. Subjects with pre-diabetes might nevertheless profit from preventive efforts reducing their cardiovascular risk profile because cardiovascular and kidney disease share common risk factors.

Sleep Apnea and Glucose Metabolism: A Long-term Follow-up in a Community-Based Sample

It has been suggested that sleep-disordered breathing (SDB) is a risk factor for diabetes, but long-term follow-up studies are lacking. The aim of this community-based study was to analyze the influence of SDB on glucose metabolism after > 10 years. Men without diabetes (N = 141; mean age, 57.5 years) were investigated at baseline, including whole-night respiratory monitoring. After a mean period of 11 years and 4 months, they were followed up with an interview, anthropometric measurements, and blood sampling. Insulin resistance was quantified using the homeostasis model assessment of insulin resistance (HOMA-IR). ΔHOMA-IR was calculated as (HOMA-IR at follow-up − HOMA-IR at baseline). An oral glucose tolerance test was performed on 113 men to calculate the insulin sensitivity index. The mean apnea-hypopnea index (AHI) and oxygen desaturation index (ODI) at baseline were 4.7 and 3.3, respectively. At follow-up, 23 men had diabetes. An ODI > 5 was a predictor of developing diabetes (OR, 4.4; 95% CI, 1.1-18.1, after adjusting for age, BMI, and hypertension at baseline and ΔBMI and years with CPAP during follow-up). The ODI was inversely related to the insulin sensitivity index at follow-up (r = −0.27, P = .003). A deterioration in HOMA-IR was significantly related to all variables of SDB (AHI, AHI > 5; ODI, ODI > 5; minimum arterial oxygen saturation), even when adjusting for confounders. When excluding the variable years with CPAP from the multivariate model, all associations weakened. SDB is independently related to the development of insulin resistance and, thereby, the risk of manifest diabetes mellitus.

Fasting plasma glucose and HbA1c in cardiovascular risk prediction: a sex-specific comparison in individuals without diabetes mellitus

This study aimed to assess the cardiovascular risk of individuals with fasting plasma glucose (FPG)- and/or HbA(1c)-defined prediabetes (5.6-6.9 mmol/l and 39-47 mmol/mol [5.7-6.4%], respectively) or manifest diabetes mellitus and to evaluate whether FPG or HbA(1c) can improve risk prediction beyond that estimated by the Systematic Coronary Risk Evaluation (SCORE) chart in individuals without diabetes mellitus. Cox regression was employed to estimate HRs for primary incident cardiovascular events (CVEs) in a cohort of 8,365 individuals aged 50-74 years. Furthermore, HbA(1c) and FPG were added individually to the variables of the SCORE and measures of model discrimination and reclassification were assessed. During 8 years of follow-up, 702 individuals had a primary CVE. After adjusting for conventional cardiovascular risk factors, HRs were attenuated close to one for the prediabetes groups (especially for women), whereas a 1.7- and a 1.9-fold increased risk persisted for men and women with diabetes, respectively. Extension of the SCORE variables by either FPG or HbA(1c) did not improve its predictive abilities in individuals without diabetes. There was a non-significant net reclassification improvement for men when HbA(1c) was added (2.2%, p = 0.16). The increased cardiovascular risk of individuals with FPG- or HbA(1c)-defined prediabetes can mainly be explained by other cardiovascular risk factors. Adding FPG or HbA(1c) did not significantly improve CVE risk prediction by the SCORE variables in individuals without diabetes mellitus.

Neuropathy in prediabetes: does the clock start ticking early?

Between 25% and 62% of patients with idiopathic peripheral neuropathy are reported to have prediabetes, and among individuals with prediabetes 11-25% are thought to have peripheral neuropathy, and 13-21% have neuropathic pain. Population-based studies suggest a gradient for the prevalence of neuropathy, being highest in patients with manifest diabetes mellitus, followed by individuals with impaired glucose tolerance then impaired fasting glucose and least in those with normoglycemia. The most sensitive test to assess glucose metabolism status is the oral glucose tolerance test. Pathogenesis involves hyperglycemia, microvascular abnormalities, dyslipidemia and the metabolic syndrome. Individuals with prediabetes have less severe neuropathy than those with manifest diabetes mellitus. Sensory modalities are more frequently affected than motor modalities, but impairment of small nerve fibers could be the earliest detectable sign. Diagnosis should rely on careful clinical examination, with emphasis on the evaluation of small fibers. An oral glucose tolerance test should be performed in patients with idiopathic neuropathy. The only treatment with any efficacy is lifestyle modification to improve control of hyperglycemia and cardiovascular risk factors, but long-term efficacy of this approach has not been established. This Review summarizes the current evidence on the association between prediabetes and neuropathy.

DO ANTIOXIDANT VITAMINS AMELIORATE THE BENEFICIAL EFFECTS OF EXERCISE TRAINING ON INSULIN SENSITIVITY?

Purpose: Exercise training has numerous health benefits, and in patients with type 2 diabetes mellitus and metabolic syndrome, it can improve insulin sensitivity and glucose control. A recent publication suggests that antioxidant vitamins (C and E) block these effects on blood glucose. This investigation was undertaken to determine whether antioxidant vitamins ameliorate the beneficial effects of cardiac rehabilitation and exercise training (CRET) on insulin sensitivity and glucose metabolism in patients with coronary heart disease (CHD). METHODS:: We assessed CHD risk factors, including clinical indices of glucose metabolism, and evaluated the effects of exercise training in 315 patients with CHD with diabetes mellitus and/or metabolic syndrome before and after a 3-month program of CRET. Patients were divided into 2 groups based on self-reported antioxidant vitamin (vitamins C and E) consumption. RESULTS:: Both groups, 113 patients (36%) consuming vitamins (Vits group) and 202 patients (64%) who reported no vitamin use (no-Vits group) were statistically similar at baseline. Following CRET, patients improved exercise capacity (+10%, P < .0001), fasting blood glucose (-7%, P < .0001), percent body fat (-3%, P < .0001), high-sensitive C-reactive protein (-31%, P = .003), and various lipids and behavioral parameters, but there was no significant improvement in glycosylated hemoglobin following formal CRET. Both Vits group and no-Vits group achieved statistically similar improvements in fasting blood glucose, body fat, and other CHD risk factors. Conclusions: Commercially available antioxidant supplements (mean dose of 400 IU of vitamin E and 500 mg of vitamin C) do not ameliorate the health benefits of exercise training, including fasting blood glucose, in CHD patients with manifest diabetes mellitus and/or metabolic syndrome.

Indices of Mineral Metabolism in Subjects with an Impaired Glucose Tolerance

An altered mineral metabolism has been described both in insulin dependent and non-insulin dependent diabetes mellitus. In order to investigate if a disturbed mineral homeostasis was an early feature in the development of diabetes, 52 middle-aged men who all had recently developed an impaired glucose tolerance (IGT) were compared to healthy control persons. The IGT subjects showed higher levels of serum calcium (2.38 +/- 0.081 mmol/l (SD) vs 2.35 +/- 0.065 in controls) but similar levels of plasma ionized calcium indicating an increased protein binding of serum calcium in IGT. Serum magnesium was significantly lower in the IGT subjects (0.79 +/- 0.060 mmol/l vs 0.85 +/- 0.065, p less than 0.001) while serum phosphate was unaltered. This study demonstrates indices of an impaired mineral metabolism in IGT subjects similar in characteristics to what has previously been reported in manifest diabetes mellitus suggesting that an alteration of mineral homeostasis could be part of a primary event.

Glucose metabolism and liver cirrhosis.

Chronic liver disease is characterized by numerous metabolic alterations, predominantly catabolic, resulting in the clinical picture of malnutrition and even cachexia in some patients. The following review focuses on disturbances of glucose metabolism and of hormonal interactions that could contribute to the clinical picture of malnutrition seen in chronic liver disease. Body composition is altered in a characteristic manner with an increase in fat mass and a significant loss of muscle tissue. Furthermore, defective glucose storage due to reduced insulin sensitivity predominantly of muscle tissue has been observed. The pathogenesis of insulin resistance leading to an impaired glucose tolerance or a manifest diabetes mellitus is as yet unknown. A receptor/postreceptor dysfunction probably exists in chronic liver disease that might be explained by the following factors: 1. Altered membrane lipid composition and increased levels of free fatty acids; 2. long-lasting hyperinsulinemia; 3. increased plasma levels of insulin counteracting hormones such as growth hormone, glucagon, catecholamines and possibly cytokines; 4. a lack of liver-derived humoral factors with insulin-like activity, i.e. insulin-like growth factors I and II.