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PubMed2026

Validating the potential mechanism and therapeutic effect of Qinlian Jiangxia decoction in the treatment of type 2 diabetes mellitus complicated with hyperlipidemia through network pharmacology, molecular docking, molecular dynamics simulation, andexperiments.

OBJECTIVE: To investigate the mechanism of action of Qinlian Jiangxia decoction (, QLJXD) in the treatment of type 2 diabetes mellitus (T2DM) complicated by hyperlipidemia using network pharmacology, molecular docking, molecular dynamics simulation and in vivo experiments. METHODS: Drug components, targets and disease targets were identified using databases such as TCM systems pharmacology database and analysis platform and GeneCards. The intersecting targets were subjected to protein-protein interaction analysis using the search tool for the retrieval of interacting genes/proteins database. Subsequently, Gene Ontology and Kyoto Encyclopedia of Genes and Genomes analysis of the intersecting targets were conducted using the Metascape platform to identify core components and targets. The results were validated using molecular docking, molecular dynamics simulations and in vivo experiments. RESULTS: QLJXD contains 76 active ingredients and 136 disease targets. The core ingredients are quercetin, β-sitosterol, wogonin and baicalein, while the core targets are fatty acid binding protein 4 (FABP4) and peroxisome proliferative activated receptor gamma (PPARG). Molecular docking and molecular dynamics simulations revealed that the core ingredients bound well to the core targets. Animal experiments demonstrated that QLJXD effectively inhibited the expression of FABP4 and increased the expression of PPARG, thereby enhancing disorders of glycolipid metabolism. CONCLUSION: The putative therapeutic efficacy of QLJXD in the management of T2DM complicated with hyperlipidemia may be ascribed to the synergistic actions of multiple components, such as quercetin, β-sitosterol, wogonin, and baicalein, which collectively modulate FABP4 and PPARG molecular targets.

Molecular Docking Simulation↗
PubMed2006

Fine tuning of PPAR ligands for type 2 diabetes and metabolic syndrome.

Type 2 diabetes mellitus (T2DM) is highly prevalent chronic disease. Recently, many biological targets are discovered for treatment of this disease. The identification of the nuclear hormone receptor peroxisome proliferator activated receptors (PPAR) and their subtypes alpha, gamma and delta or beta as targets for controlling lipid, glucose and energy homeostasis has proved to be exciting. As hyperlipidaemia, obesity and insulin resistance are independent risk factors for coronary heart disease and macrovascular complications of diabetes; new agents that increase insulin sensitivity as well as decrease hyperlipidaemia by distinct yet complementary mechanism are being studied as they may provide improved therapy for T2DM and related disorders. In this article, we review highly potent PPARgamma agonists, PPARalpha/gamma dual agonists, PPAR pan agonists, alternative PPAR ligands like partial agonists or selective PPAR modulators (SPPARMs) and antagonists from a chemist point of view.

Antioxidants↗
PubMed2006

Rosiglitazone increases LDL particle size and buoyancy and decreases C-reactive protein in patients with type 2 diabetes on statin therapy.

A substantial number of individuals with type 2 diabetes mellitus (T2DM) demonstrate a predominance of small dense low-density lipoprotein (sdLDL), which is associated with an increased risk of cardiovascular disease (CVD). In some cases, sdLDL persists after treatment with a statin to reduce levels of LDL. The effect of the addition of a thiazolidinedione, rosiglitazone (RSG) (4 mg/day or 8 mg/day) to statin therapy on LDL phenotype and C reactive protein (CRP) levels was investigated in a 12- week, placebo-controlled study of 72 T2DM patients who were well controlled and on a statin, but who had persistently predominant sdLDL. Addition of RSG 8 mg to statin therapy significantly increased LDL buoyancy (relative flotation +0.014, p = 0.003) and LDL particle size (+4.2A, p = 0.001) from baseline and relative to the change with placebo (+0.014 and +3.8A; p = 0.03 and p = 0.04, respectively), and was associated with a non-significant decrease in sdLDL. RSG 8 mg moderately, but significantly, increased total cholesterol (by 12.2%, p = 0.004), LDL-cholesterol (11.2%, p = 0.02) and intermediate-density lipoprotein (IDL)-cholesterol from baseline but did not increase total or LDL apolipoprotein B. RSG 4 mg and 8 mg significantly reduced CRP compared with placebo (-44.9% and -48.0%; p = 0.008 and p = 0.004, respectively), and significantly reduced insulin resistance and fasting plasma glucose from baseline. Addition of RSG to statin therapy may further reduce cardiovascular risk by improving the LDL phenotype, as well as reducing insulin resistance and CRP levels. However, the increase in IDL may be proatherogenic and must be considered when assessing the benefits of rosiglitazone.

Blood Glucose↗
PubMed1999

Glucose tolerance and insulin secretion in pregnancy.

The authors have studied the behaviour of plasma glucose, insulinaemia and insulin-glucose ratio in 2 groups of pregnant women with BMI values > or = or <26, respectively. Each group was divided into 3 subgroups on the basis of an oral glucose tolerance test (OGTT) response: GIGT (gestational impaired glucose tolerance), GD (gestational diabetes), and C (normal controls). Data from non-obese pregnant women demonstrate that both basal and OGTT-stimulated glucose levels were significantly different in all subgroups. The total insulin amount in the GIGT and GD subgroups is quite similar to or greater than the controls, but with a significant reduction of the insulin-glucose ratio. In GD also an absolute deficiency of insulin rise at 30 min during the glucose load, as in subjects with Type 2 diabetes mellitus (T2DM), was observed. The behaviour of these parameters in obese pregnant women seems to be similar, even though with some significant differences: in these subjects, there is a less clear-cut differentiation among all subgroups, and the appearance of gestational diabetes is not accompanied by a significant decrease of insulin secretion at 30 min. Our data seem to demonstrate that insulin resistance with an inadequate hyperinsulinaemia is a common factor for the alterations of carbohydrate metabolism during pregnancy. Only in the non-obese patients with gestational diabetes, is there an absolute defect of early insulin response to the glucose load, as it is seen in T2DM.

Adult↗
PubMed2000

The clinical utility of QT interval assessment in diabetes.

A prolonged (QT) interval is considered an indicator of an increased risk of malignant ventricular arrhythmias and/or sudden death. It has been proposed that autonomic neuropathy in diabetes is related to QT interval prolongation and higher mortality rates. More recently, the interlead difference in QT interval duration has been referred to as QT interval dispersion, which has proven to be predictive of ventricular arrhythmias and mortality in different groups of patients. QT interval duration and dispersion are significantly related, but are not concordant in a substantial number of cases in identifying patients at risk. The prevalence of QT prolongation in Type 1 and Type 2 diabetic (T1 and T2DM) patients is higher than 20%. Several studies in T1 and T2DM patients have confirmed the independent relation between prolonged QT interval duration and increased QT interval dispersion and chronic ischemic heart disease. It has been consistently shown that autonomic neuropathy is related to QT interval duration, while more controversies exist on the association with QT interval dispersion. In recent years 5 studies have been published which confirm the value of QT interval as a predictor of total mortality in diabetic as well as in non-diabetic subjects. Surprisingly, no data exist on the relation between the risk of sudden death and QT interval prolongation in diabetic patients. As corrected QT interval is significantly related to mortality, it could be used to stratify the death risk in diabetic patients, particularly those who are candidates for surgery or kidney and/or pancreas transplantation. We still do not know why QT interval is prolonged and how this abnormality leads to death: however, a simple, low-cost measurement, which is easily obtainable without the need of the patient's compliance, could help select patients who need second level diagnostic procedures and strict observation.

Arrhythmias, Cardiac↗
PubMed2001

Insulin therapy may increase blood pressure levels in type 2 diabetes mellitus.

OBJECTIVE: To assess the effects of insulin therapy on blood pressure levels in type 2 diabetes mellitus (T2 DM). MATERIAL AND METHODS: This is a retrospective analysis of clinical records of 313 T2DM patients (125 men and 188 women), excluding those with proteinuria or hypertensive diseases and those taking drugs that may influence blood pressure levels except antihypertensive therapy. Mean age was 56.3 +/- 11.7 years and mean duration of diabetes was 7.1 +/- 5.5 years. After one week of observation under diet and maximal doses of oral antidiabetic drugs, patients who did not improve their glucose control were changed towards insulin therapy (n=129) and formed the insulin treated group (ITG), those who improved their glucose levels were maintained under oral therapy (n=184) and formed the orally treated group (OTG). Blood pressure levels were compared between the two groups at baseline and after a mean follow-up period of 12.1 +/- 6.1 months. Hypertension was considered if patients were known and treated or if SBP >=140 mmHg and/or DBP >=90 mmHg. RESULTS: At baseline, patients in ITG were moderately older (58.4 +/- 11 vs 54.9 +/- 12.1 years, p<0.05), had a longer duration of diabetes (9.2 +/- 6.2 vs 5.7 +/- 5 years, p<0.01), a lower BMI (24.6 +/- 4.6 vs 28.8 +/- 6.6 kg/m(2), p<0.01) and a higher frequency of retinopathy (44% vs 31.1%, p<0.05). There was no significant difference regarding sex ratio, WHR, family history of hypertension, plasma levels of creatinine and lipid parameters. SBP, DBP and frequency of hypertension were similar in both groups at baseline. After follow up, insulin treated group exhibited higher levels of SBP (150 +/- 25.7 vs 138.6 +/- 27.1 mmHg, p<0.001) and DBP (84.1 +/- 13 vs 75.8 +/- 14.9 mmHg, p<0.001) than orally treated group. Progression rate of hypertension frequency was mildly but not significantly higher in ITG than in OTG (+21% vs +12%, p=0.08) and was associated with weight gain in ITG only. SBP increase was mildly correlated with weight gain (p=0.06). In ITG, higher values of BMI (> 27 kg/m(2)) at baseline were associated with the highest increases of blood pressure levels under insulin therapy. No significant relationship was found with insulin doses. CONCLUSION: Insulin therapy may contribute to the development of hypertension in T2DM obese patients. Additional prospective randomised studies are required for a better appreciation of such influence.

Adult↗
PubMed2002

Allelic variation in exon 18 of the sulfonylurea receptor 1 (SUR1) gene, insulin secretion and insulin sensitivity in nondiabetic relatives of type 2 diabetic subjects.

BACKGROUND: We have previously observed associations of the T-allele of the exon 18 variant (ACC --> ACT; Thr759Thr) of the sulfonylurea receptor 1 (SUR1) gene with type 2 diabetes mellitus (T2DM). Here we assess beta-cell function and insulin sensitivity in carriers of different genotypes at this locus. METHODS: Pre-hepatic insulin secretion rates (ISR) derived by deconvolution of circulating C-peptide levels, and glucose clearance were assessed during graded infusions of intravenous glucose in CC-homozygous (n=6) and CT-heterozygous (n=6) nondiabetic relatives of CT-heterozygous type 2 diabetic subjects. RESULTS: Average ISR over the duration of the study, adjusted for sex, age, BMI and prevailing glucose levels, were lower in CT-heterozygous subjects as compared with CC-homozygous subjects (3.91 +/- 0.40 vs. 4.84 +/- 0.28 pmol/kg x min(-1); p=0.048). The correlation curves relating ISR to glucose levels were significantly different in the two groups (analyses of covariance p=0.029). Glucose clearance was similar in both groups. CONCLUSIONS: Insulin secretion rates, but not insulin sensitivity, assessed during graded infusion of glucose were mildly decreased in nondiabetic relatives of type 2 diabetic subjects, who carry the at risk T-allele of exon 18 variant of the SUR1 gene. These results suggest that the at-risk allele might have a small effect on pancreatic B-cell function and contribute to the development of T2DM in these families.

ATP-Binding Cassette Transporters↗
PubMed2002

Therapeutic strategies for Type 1 and Type 2 diabetes mellitus.

Although diabetes mellitus is a manageable disorder, the associated complications that result in significant morbidity and mortality worldwide necessitate novel approaches of pharmacologic, cell, and gene therapy for an eventual cure. A significant number of animal studies have demonstrated the potential of restoring normoglycemia by islet transplantation in the context of immunoregulation achieved by gene transfer of immunoregulatory genes to allo- and xenogeneic islets ex vivo. Examples include viral vector-mediated gene transfer of immunosuppressive cytokines, proteins that block co-stimulation and molecules that prevent apoptotic cell death. Additionally, gene and cell therapy has also been used to induce tolerance to auto- and alloantigens and to generate the tolerant state in autoimmune rodent animal models of Type 1 diabetes mellitus (T1DM) or rodent recipients of allogeneic/xenogeneic islet transplants. Gene transfer of putative autoantigens is one example. The achievements of gene and cell therapy in Type 2 diabetes mellitus (T2DM) are less evident, but seminal studies promise that this modality can be relevant to treat and perhaps prevent the underlying causes of the disease including obesity and insulin resistance. Herein, we present an overview of the current status of drug, gene and cell therapy for T1DM and T2DM and we propose novel therapeutic options that could be clinically useful.

Animals↗
PubMed2002

Early-phase prandial insulin secretion: its role in the pathogenesis of type 2 diabetes mellitus and its modulation by repaglinide.

The major contributory factor to increasing hyperglycaemia in established Type 2 diabetes mellitus (T2DM) appears to be the progressive delay and attenuation of the prandial insulin response. An important consequence of this derangement is that hepatic glucose production is no longer suppressed during times of prandial glucose intake. Together with a relative impairment in the rate of peripheral glucose disposal, this leads to supra-physiological plasma glucose excursions, which may damage the vasculature. An obvious therapeutic strategy, therefore, would be to increase insulin availability when most needed--in the early prandial phase. In experiments with exogenous insulin interventions, peak post-prandial blood glucose increments were curtailed without undue increases in total insulin exposure. However, available evidence suggests that the sulphonylurea glibenclamide does not effectively alter early-phase prandial insulin release but predominately increases late-phase and basal insulin output, thus incurring the risk of hypoglycaemia. The novel insulin secretagogue repaglinide, by contrast, augments early-phase prandial insulin secretion when taken before meals, as shown by studies in non-diabetic people and patients with newly diagnosed, previously untreated T2DM. Repaglinide exerts its greatest effect on the insulin secretion rate during the first 30 min after a meal is started, thereby going some way to restoring the early insulin secretion curve seen after a meal in non-diabetic people. No residual secretagogue activity is seen 4 hr after taking a single dose of up to 2 mg. Prandial glucose regulation with repaglinide could be associated with lower post-prandial glucose excursions and less risk of post-prandial hypoglycaemia than glibenclamide.

Area Under Curve↗
PubMed2002

Repaglinide in combination therapy.

Type 2 diabetes mellitus (T2DM) is a progressive disorder requiring increasingly aggressive treatment to achieve and maintain target blood glucose concentrations in the presence of deteriorating insulin secretion and increasing insulin resistance. Diet and lifestyle modification are often sufficient initially; however, most patients eventually require pharmacological intervention. With disease progression, monotherapy becomes less effective, so combination therapy is required, using drugs with complementary modes of action to maximise glycaemic control. The prandial glucose regulator repaglinide has been studied in combination with metformin (an inhibitor of hepatic glucose production), neutral protamine Hagedorn (NPH)-insulin (which has a long duration of effect, but at the risk of early hypoglycaemia and late hyperglycaemia in the dosing interval) and three thiazolidinediones (TZDs--troglitazone, rosiglitazone and pioglitazone, which stimulate nuclear receptors to increase insulin sensitivity and reduce insulin resistance) in patients whose diabetes was inadequately controlled by previous monotherapy or combination therapy. The combination of repaglinide and metformin resulted in reduced fasting plasma glucose concentrations (by 2.2 mmol/l) and HbA1c (by 1.4%). Combination therapy with repaglinide and bedtime NPH-insulin resulted in reductions in fasting plasma glucose (by 5.4 mmol/l) and HbA1c (by 0.7%). The combination of repaglinide and each TZD also resulted in consistent decreases in fasting plasma glucose concentrations and HbA1c. No severe hypoglycaemic episodes were reported in the three studies. In conclusion, repaglinide has additive, and often synergistic, effects on glycaemic control when given in combination regimens and should be a valuable option in the management of patients with T2DM.

Carbamates↗
PubMed2003

[Association of autoantibody and cytokines with latent autoimmune diabetes in adults].

OBJECTIVE: To assess the clinical value of detecting glutamic acid decarboxylase antibody (GADA), islet cell antibody (ICA) and cytokines in the diagnosis of latent autoimmune diabetes in adults (LADA), and define the characteristics of the two different types of LADA. METHODS: A total of 500 patients with an initial diagnosis of type 2 diabetes mellitus (T2DM) were tested for GADA, ICA and cytokines by enzyme-linked immunosorbent assay. RESULTS: In type 2 diabetic patients approximately 11% were positive for GADA, who had similar symptoms as hypertension, hyperlipidemia and other diabetic complications to justify the diagnosis of LADA-2 subtype. Another 9.6% of the total patients were ICA-positive, and when compared with T2DM, these patients had similar clinical findings typical of type 1 diabetes such as younger age of onset, impaired beta cell function and dependence on insulin treatment. Therefore they had more resemblance to insulin-dependent diabetes and can be diagnosed as having LADA-1 subtype. It was also found that cytokines positively acted on GADA and ICA, showing positive correlation between them. CONCLUSION: LADA has LADA-1 and LADA-2 subtypes, and GADA, ICA and cytokines test have important clinical significance for diagnosis of LADA.

Adult↗
PubMed2003

[Metabolic syndrome and latent autoimmune diabetes in adults].

OBJECTIVE: To investigate the prevalence of metabolic syndrome (MS) in latent autoimmune diabetes in adults (LADA) and to study the positivity of glutamic acid decarboxylase autoantibody (GADA) in diabetic patients with MS. METHODS: Sera of 598 patients with an initial diagnosis of type 2 diabetes (T2DM) were screened for GADA with radioligand assay. These patients were divided into LADA and T2DM groups according to the titers of GADA to compare the prevalence of MS; the proportions of LADA in diabetic patients with and without MS were studied. We also compared the clinical characteristics of LADA patients with and without MS. RESULTS: About 23.7% of the LADA patients had MS. In patients with MS, the prevalence of LADA was 10.0%, of which approximately 95% had low GADA titers, that was, belonging to LADA-type 2. Compared with LADA patients with MS, LADA without MS were similar to classical type 1 diabetes and had features of low body weight, tendency to develop ketosis and impaired islet cell function. CONCLUSION: About 23.7% patients with MS are found in LADA patients. The GADA levels in LADA patients with and without MS are significantly different, which may need different therapeutic strategies.

Adolescent↗
PubMed2004

[Adult-onset latent autoimmune diabetes and autoimmune thyroid disease].

OBJECTIVE: To investigate the relationship between latent autoimmune diabetes in adults (LADA) and thyroid autoimmunity. METHODS: The frequency of thyroid peroxidase antibody (TPO-Ab) and thyroglobulin antibody (TG-Ab) was determined with radioimmunoassay in 394 subjects, including 90 LADA, 104 classic type 1 diabetics (T1DM), 100 type 2 diabetics (T2DM) and 100 controls. Glutamic acid decarboxylase antibody (GAD-Ab) was measured with radioligand immunoassay. RESULTS: (1) TPO-Ab existed more frequently in LADA (16.7%, 15/90) than in T2DM patients (7.0%, 7/100; P < 0.05). The frequency of thyroid antibody (TPO-Ab or TG-Ab positivity) in LADA and T1DM was 18.9% (17/90) and 25.0% (26/104) respectively, being higher than that in the control group (8/100, 8.0%; P < 0.05). (2) Thyroid antibodies occurred more frequently in LADA patients with higher titer of GAD-Ab (GAD-Ab > or = 0.5) than those with lower ones (50.0% vs 12.5%, P < 0.05). (3) 47.1% (8/17) of LADA patients with thyroid autoimmunity had thyroid dysfunction as compared with 17.6% (6/34) in the group without thyroid antibodies (P < 0.05). CONCLUSIONS: (1) LADA patients, especially those with high titer of GAD-Ab, have high risk for thyroid autoimmunity. (2) The presence of thyroid antibody may predict high risk for thyroid dysfunction in LADA patients. (3) LADA may be one of the components in autoimmune polyendocrine syndrome.

Adolescent↗
PubMed2004

Prevalence of osteoporosis among postmenopausal females with diabetes mellitus.

OBJECTIVE: To assess the prevalence of osteopenia and osteoporosis among Saudi postmenopausal women with non-insulin dependent type 2 diabetes mellitus (T2DM). METHODS: The study was carried out at King Khalid University Hospital, Riyadh, Kingdom of Saudi Arabia from February 2000 to September 2002. Bone mineral density (BMD) of the lumbar spine and femoral neck using dual x-ray absorptiometry (DXA; Lunar Wisconsin), were performed in 104 postmenopausal Saudi women with T2DM, and 101 postmenopausal non-diabetic women (control). Bone mineral density was measured in gm/cm2 and both T-score and Z-score were measured but only T-score was used for analysis based on World Health Organization criteria. Bone profile, 25(OH) Vitamin D, 1,25(OH)2 Vitamin D, parathyroid hormone and urine deoxypyridinoline (DPD) were measured in most patients and controls. Body fat measurement around the biceps muscles using Futrex (body composition analyzer) were performed in patients and controls. Years postmenopausal, duration of diabetes mellitus, parity, exercise, sun exposure and milk consumption were also recorded. RESULTS: In the diabetic group, the mean spine BMD was 0.928 gm/cm2 (T-score = -2.28 SD) and for femoral neck the mean BMD was 0.817 gm/cm2 (T-score = -1.21 SD). In control group, the mean spine BMD was 1.036 gm/cm2 (T-score = -1.2) and mean femoral neck BMD was 0.914 gm/cm2 (T-score = -0.608). In the diabetic group, there was 16 (16.64%) patients with normal BMD of the spine, 42 patients (43.68%) with osteopenia (mean T-score = -1.8 SD) and 45 (46.8%) with osteoporosis (mean T-score = -3.3 SD). CONCLUSION: Osteoporosis is more common among Type 2 postmenopausal females in this ethnic group. Since both groups are postmenopausal, having equal percentage of Vitamin D deficiency, multi-parity, non exposure to sun, lack of exercise and negligible milk intake, one can conclude that the low BMD can be attributed to DM in the absence of other causes of osteoporosis.

Absorptiometry, Photon↗
PubMed2004

Effects of timely insulin treatment on protection of beta cells in a rat model of type 2 diabetes mellitus.

BACKGROUND: Insulin treatment plays a key role in management of diabetes mellitus. Clinical researches showed that extra improvements in restoration of insulin secretion of pancreatic beta cells were found in patients with newly diagnosed type 2 diabetes. The purpose of this study was to investigate the effects of early insulin treatment on insulin mRNA expression and morphological alterations of beta cells in a Sprague Dawley (SD) rat model of type 2 diabetes. METHODS: A rat model of type 2 diabetes mellitus (T2DM) was induced by a high fat diet (high energy, HE) and low doses of streptozotoxin (STZ, 40 mg/kg). A group of diabetic rats was then injected with protamine zinc insulin [PZI, 1 - 2 U x kg(-1) x d(-1)] for one week. Insulin mRNA expression, morphological features of pancreatic islets, and metabolic parameters were examined in rats using reverse transcriptase-polymerase chain reaction (RT-PCR), immunohistochemistry, and other techniques. RESULTS: In insulin-treated diabetic rats, insulin mRNA levels prominently increased by 81.3% (P < 0.05), as compared with untreated diabetic rats. Moreover, timely insulin treatment noticeably improved the insulin content of beta cells, with an increase of 10.2% (P < 0.05), despite a slight reduction in fasting blood glucose (FBG), triglyceride (TG), and free fatty acid (FFA) levels, as compared to an untreated diabetic group. CONCLUSION: Insulin treatment at the onset of T2DM effectively improves insulin synthesis, as confirmed by morphological changes to beta cells in a rat model of type 2 diabetes.

Adipose Tissue↗
PubMed2004

NIDDM: new once-daily intervention for type 2 diabetes mellitus: Diaprel MR.

UNLABELLED: Pharmacological treatment of hyperglycemia should address to both abnormalities in T2DM treatment, that is reduction of insulin resistance and restoration of normal insulin secretion. Gliclazide is a sulfonylurea compound oral hypoglycemic drug that has a unique feature of restoring the first-phase insulin secretion, which is lost in T2DM being one of the early features of disease. MATERIAL AND METHOD: Laboratoires Servier conducted in Romania a an open non randomized surveillance on the efficacy and safety of Diaprel MR in type 2 diabetic patients. 199 patients in 14 treatment centers were enrolled. Eligibility criteria were as it follows: men and women with diabetes, previously on diet alone and not treated with other OAD, over 35 years old with FPG (mg/dl) at enrollment between 126 and 180. The clinical trial lasted for 16 weeks. During this period the doctors examined the patients 6 times. First visits were at a 2 weeks interval and the last two visits at a 4 weeks interval. At each visit the doctor renewed the prescription for the subsequent period according to the following protocol: the starting dose was 30 mg Diaprel MR/day, if the FPG (mg/dl) was over 140 (at the next visit) the dosage was increased with 30 mg Diaprel MR/day, if the FPG (mg/dl) was under 140 the dosage remained the same as the previous dosage. The maximum dosage was 120 mg Diaprel MR/day. The following parameters were measured on first and last (seventh) visit: blood pressure (systolic and diastolic), heart rate (bpm), body mass index-BMI (kg/m2), fasting plasma glucose FPG (mg/dl and mmol/l), glycated hemoglobin HbA1c (%) and Hb-Hct (mg/dl-%), creatinine (mg/dl), SGPT (UI/I), cholesterol (mg/dl) and triglycerides (mg/dl). Blood pressure (systolic and diastolic), heart rate, BMI and FPG were measured from the second to sixth visit also. On each visit there was registered other data such as: associated illnesses, concomitant medication and adverse events. RESULTS: Primary end points. The average values of end points HbA1c (%) and PFG (mg/dl) registered a significant decrease during the 16 weeks of medication, from the enrollment moment (S0) to the last week (S16). The decrease was significant on the total sample of the main analysis group but also on subsamples of age, gender and BMI. HbA1c (%) average values decreased in the main analysis group (S16 compared to S0): with 22% on the total sample (from 7.7 to 6.0); p < 0.05. FPG (mg/dl) average values decreased in the main analysis group (S16 compared to S0): with 21% on the total sample (from 159 to 126); p < 0.05. Secondary end points. There were no significant changes registered in the average level of cholesterol and triglycerides, BMI, diastolic blood pressure, heart rate, creatinine, SGPT. A significant decline of the average systolic blood pressure was registered. CONCLUSION: Diaprel MR can be used safely in diabetic patients newly diagnosed, uncontrolled on diet or other oral antidiabetic drugs, overweight, safely in those with cardio-vascular disease, or in patients with creatinine clearance 50-80 ml/min.

Adult↗
PubMed2004

Diabetes in children and young adults in Waikato Province, New Zealand: outcomes of care.

BACKGROUND: Diabetes is an important cause of morbidity and mortality among young people. Despite improvements in technology, maintenance of good glycaemic control is hard to achieve particularly during the teenage years. AIMS: To assess the outcomes of care in young people aged under age 26 years with diabetes living in New Zealand's Waikato District Health Board (DHB) area. METHODS: Audit of health records. RESULTS: Two hundred and fifty-one patients who had attended an outpatient consultation at least once in the last 3 years were identified. The mean HbA1c was 9.2% (CI 8.8-9.8). There were no gender differences. The prevalence of retinopathy was 13%, and nephropathy up to 19%. Eleven patients were taking ACE inhibitors and one person had end-stage renal failure treated with continuous ambulatory peritoneal dialysis (CAPD). Forty percent of those patients over 10 years of age had a low density lipoprotein (LDL) cholesterol level of >2.6mmol/L. All of those patients with type 2 diabetes mellitus (T2DM) were overweight, compared to 28% of those patients with type 1 diabetes mellitus (T1DM). CONCLUSIONS: These results confirm the difficulty of achieving good glycaemic control in children and young adults. Microvascular complications are common, particularly in those of long duration. Risk factors for macrovascular disease are present from an early age, especially in those with T2DM. It is likely that these outcomes of care are typical for children and young adults with diabetes in New Zealand.

Adolescent↗
PubMed2005

[Effects of rosiglitazone on aortic function in rats with insulin resistant-hypertension].

Rosiglitazone (ROSI), thiazolidione peroxisome proliferator-activated receptor-gamma (PPAR-gamma) activator, reduces insulin resistance in patients with type 2 diabetes (T2DM). It also improves vascular reactivity in T2DM patients and some animal models by unclear mechanisms. In order to investigate the effect of ROSI on aortic systolic and diastolic function of insulin resistant-hypertensive rats (IRHR) and the underlying mechanism, male Sprague-Dawley (SD) rats were fed with high fructose (HF) for 8 weeks to induce IRHR model. To verify IRHR model, systolic blood pressure (SBP), fasting blood sugar (FBS), fasting serum insulin (FSI) were measured respectively in each group, and insulin sensitive index (ISI) was also calculated. Subsequently, the vascular function test was performed. The thoracic aortic ring of SD rats was mounted on a bath system. The effect of rosiglitazone on the contraction elicited by L-phenylephrine (PE) and potassium chloride (KCl) and the relaxation induced by acetylcholine (ACh) and sodium nitroprusside (SNP) were measured. To explore the mechanism, nitric oxide synthase (NOS) inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) was used and serum nitric oxide (NO) was measured. The results obtained were as follows: (1) Rosiglitazone reduced the level of SBP, serum insulin and improved insulin resistance in IRHRs. (2) The contractive responses of thoracic aortic rings to PE and KCl were enhanced and the relaxation response to ACh was depressed significantly in the HF group, and the effect was reversed by ROSI. (3) After pretreatment with L-NAME, the relaxation response to ACh was further impaired in the HF group, this effect was partly reversed by ROSI. (4) Sodium nitroprusside (SNP)-induced vasodilator responses did not differ significantly among the groups. (5) Aortic systolic and diastolic function of the control group was not affected markedly by ROSI. (6) Compared with the control group, serum nitric oxide was significantly reduced in the HF group, but after rosiglitazone treatment it was remarkably increased. These findings suggest that ROSI can improve aortic diastolic function of insulin resistant-hypertensive rats, the mechanism of this effect might be associated with an increase in nitric oxide mediated partly by NOS pathway, a decrease in the level of blood pressure, serum insulin and the improvement of insulin resistance.

Animals↗