Changes In Serum Glucose Research Articles

Body fat distribution, serum glucose, lipid and insulin response to meals in Alström syndrome

Alström syndrome is an autosomal recessive condition characterized by obesity, insulin resistance and hypertriglyceridaemia. Responses to fat and carbohydrate ingestion are important in planning dietetic advice and may help to explain the mechanism of metabolic disorder in the syndrome. After a 12-h fast, five Alström subjects received a 3.1 MJ (742 kcal), 75.8% fat breakfast on day 1, and a 3.3 MJ (794 kcal), 77.5% carbohydrate breakfast on day 2. Serum glucose, triglyceride and insulin levels were measured at baseline, and 2 and 3.5 h post-meal. Abdominal computerized tomography in three subjects and magnetic resonance imaging in one demonstrated distribution of abdominal fat. Body fat was distributed subcutaneously, as well as viscerally. There were no changes in serum glucose, insulin or triglycerides after the high fat meal. Triglycerides remained stable after the high carbohydrate meal but glucose and log insulin levels increased [8.4 +/- 4.1 to 13.4 +/- 6.9 mmol L(-1) (P < 0.05) and 2.6 +/- 0.27 to 3.15 +/- 0.42 pmol L(-1) (P < 0.05), respectively]. Dietetic advice in Alström syndrome must include calorie restriction to reduce obesity, which is predominantly subcutaneous. This study has shown that low carbohydrate advice may prove more effective than fat restriction in control of hyperglycaemia and hyperinsulinism. A single high energy meal does not exacerbate hypertriglyceridaemia.

Long-Term Ingestion of Insoluble Dietary Fiber Increases Luminal Mucin Content, but Has No Effect on Nutrient Absorption in Rats

We reexamined the hypothesis that increased mucin secretion by the ingestion of insoluble dietary fiber (IDF) could affect small intestinal nutrient absorption. Polystyrene foam (PSF) was used as IDF. Rats were fed a diet with or without 90 g of PSF/kg for 1, 2 and 4 wk. At the end of each period, a glucose and ovalbumin (OVA) solution was intubated after 12 h of food depletion, and the changes in serum concentrations of these components were monitored. Luminal mucin was measured as O-linked oligosaccharide chains and also determined by ELISA. In all periods, the luminal mucin content was greater in the PSF-fed group than in the fiber-free control. However, the changes in serum glucose and OVA concentrations were comparable between the groups at any time during any period. These results show that the enhancement of luminal mucin secretion lasted even after chronic ingestion of IDF, but that the increased luminal mucin content had no effect on the rate of luminal nutrient absorption.

The effect of single‐dose orlistat on postprandial serum glucose, insulin and glucagon‐like peptide‐1 levels in nondiabetic obese patients

Glucagon-like peptide-1 is an insulin secretion-stimulating gut hormone that is produced in response to food intake. Orlistat (Xenical, F. Hoffman-La Roche, Basel, Switzerland), which decreases fat absorption and increases intestinal fat content, may therefore affect the secretion of glucagon-like peptide-1. In this study we examined the immediate effects of orlistat on postprandial serum glucose, insulin and glucagon-like peptide-1 levels prior to a change in body weight. Randomized, clinical study. Sixteen nondiabetic obese patients (body mass index 35.7 +/- 3.8 kg/m(2), range 32.5-43.1) were enrolled in this study. The patients were randomly assigned to either the group treated with orlistat (120 mg, single dose) or the control group. There were eight patients in each of the two groups. Orlistat was given before a standard 600-kcal mixed meal containing 60% carbohydrates, 25% lipids and 15% protein. Blood samples were collected at baseline and at 30-min intervals for 180 min after the test meal. Graphical tendencies, peak value, time to reach the peak value, and area under the curve in the two groups were compared. Blood samples were obtained for the measurement of GLP-1, glucose, insulin, high density lipoprotein, total cholesterol and triglycerides. We found no difference in sex distribution, mean age, anthropometric measurements, or baseline glucose, insulin and glucagon-like peptide-1 levels between the orlistat and placebo groups. The peak insulin and glucagon-like peptide-1 levels were determined at 60 min in the control group. Hourly changes in serum glucose and insulin levels were similar between the groups, although the peak insulin and glucagon-like peptide-1 levels were reached at 120 min in the orlistat group. There were no statistically significant differences between the groups. A single dose of 120-mg orlistat caused no change in postprandial serum glucose, insulin or glucagon-like peptide-1 levels in nondiabetic obese patients. Although glucagon-like peptide-1 increases were delayed in the orlistat group, these changes were nonsignificant.

Biosafety of recombinant and wild type nucleopolyhedroviruses as bioinsecticides.

The entomopathogenic Autographa californica (Speyer) nucleopolyhedrovirus (AcMNPV) has been genetically modified to increase its speed of kill. The potential adverse effects of a recombinant AcMNPV (AcAaIT) as well as wild type AcMNPV and wild type Spodoptera littoralis NPV (SlNPV) were studied. Cotton plants were treated with these viruses at concentrations that were adjusted to resemble the recommended field application rate (4 x 10(12) PIBs/feddan, feddan = 4,200 m2) and 3rd instar larvae of S. littoralis were allowed to feed on the contaminated plants. SDS-PAGE, ELISA, and DNA analyses were used to confirm that larvae that fed on these plants were virus-infected. Polyhedra that were purified from the infected larvae were subjected to structural protein analysis. A 32 KDa protein was found in polyhedra that were isolated from all of the viruses. Subtle differences were found in the size and abundance of ODV proteins. Antisera against polyhedral proteins isolated from AcAaIT polyhedra were raised in rabbits. The terminal bleeds from rabbits were screened against four coating antigens (i.e., polyhedral proteins from AcAaIT, AcAaIT from field-infected larvae (AcAaIT-field), AcMNPV, and SlNPV) using a two-dimensional titration method with the coated antigen format. Competitive inhibition experiments were conducted in parallel to optimize antibody and coating antigen concentrations for ELISA. The IC50 values for each combination ranged from 1.42 to 163 microg/ml. AcAaIT-derived polyhedrin gave the lowest IC50 value, followed by those of SlNPV, AcAaIT-field, and AcMNPV. The optimized ELISA system showed low cross reactivity for AcMNPV (0.87%), AcAaIT-field (1.2%), and SlNPV (4.0%). Genomic DNAs isolated from AcAaIT that were passaged in larvae of S. littoralis that were reared in the laboratory or field did not show any detectable differences. Albino rats (male and female) that were treated with AcAaIT, AcMNPV or SlNPV (either orally or by intraperitoneal injection at doses of 1 x 10(8) or 1 x 10(7) PIBs/rat, respectively) appeared to be healthy and showed increased body weight at 21 days posttreatment. The effect of virus administration on hematological, serum biochemical, and histopathological parameters were determined. Slight to moderate differences were observed in most of the hematological parameters. Specifically, serum proteins were decreased markedly in female rats treated orally with SlNPV, and in male rats injected with AcAaIT. SDS-PAGE analysis also showed some changes in serum protein profiles. No marked changes in acetylcholine esterase (AChE) activity were found. Changes in serum glucose, alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), bilirubin, creatinin, and urea were also observed. Immunohistochemical observation of tissues from stomach, intestine, liver, kidney, brain, spleen, and lung also showed slight changes. Fish (Tilapia nilotica) were also exposed to AcAaIT, AcMNPV or SlNPV by incorporating each of the viruses into diet (1 x 10(9) PIBs/group). No mortality was found in treated or untreated fish during the experimental period (28 days). Macrophage phagocytic activity of fish head kidney cells increased with time, reaching maximum values at 180 min for both treated and control fish.

Serum Glucose Changes During Insulin Therapy in Pediatric Patients With Diabetic Ketoacidosis

There are limited data on which to base insulin dosing schemes for diabetic ketoacidosis (DKA). The goal of therapy is to avoid excessive decreases in serum glucose (greater than 100 mg/dL/h) because of the risks of rapid changes in serum osmolarity and the potential risk of cerebral edema. We retrospectively reviewed the therapy of DKA in pediatric patients admitted to our Pediatric Intensive Care Unit over the past 10 years. There were 35 patients who received IV bolus insulin therapy (0.08 to 1.6 units/kg, 0.24 +/- 0.27 units/kg). The serum-glucose decrease was less than or equal to 100 mg/dL in 10 patients, 101 to 200 mg/dL in 13 patients, 201 to 300 mg/dL in 8 patients, 301 to 400 mg/dL in 2 patients, and more than 500 mg/dL in 2 patients. In patients who received 0.05 to 0.1 units/kg of insulin as a bolus dose, the decrease in serum glucose was greater than 100 mg/dL in 5 of 11 patients. An insulin infusion was administered to 91 patients. During the 243 hours of insulin infusion therapy, the decline in serum glucose was 0 to 100 mg/dL during 162 hours, 101 to 200 mg/dL during 49 hours, 201 to 300 mg/dL during 8 hours, and more than 300 mg/dL during 3 hours. Of the 193 hours of 0.05 to 0.1 units/kg/h insulin administration, there were 47 hours (24%) during which the serum-glucose decrease was greater than 100 mg/dL. Of the 21 hours of insulin administration at less than 0.05 units/kg/h, there was 1 hour (4.8%) where the serum-glucose decrease was greater than 100 mg/dL (P = 0.05 vs. insulin infusion at 0.05 to 0.1 units/kg/h). Commonly used insulin dosing regimens of a bolus of 0.1 units/kg followed by an infusion of 0.05 to 0.1 units/kg/h frequently resulted in a decrease in serum glucose of greater than 100 mg/dL/h. Prospective trials are needed to more accurately define appropriate insulin dosing regimens for pediatric patients with DKA.

Verbesserung der Myokardfunktion durch verbesserte Stoffwechselkontrolle bei Typ-2-Diabetes

In patients with type 2 diabetes mellitus diastolic dysfunction is a frequent manifestation of myocardial disease with poor prognosis. The hypothesis that better glycemic control results in improved myocardial function was tested using tissue Doppler. During a short-term (3 weeks) and a long-term (52 weeks) study, metabolic control and myocardial function were evaluated in 33 and 50 patients, respectively, with type 2 diabetes. Systolic (Vs) and diastolic (Ve) myocardial velocity were assessed by tissue Doppler. In the short-term study, antidiabetic therapy was intensified in 25 patients (Int3) and compared to those eight individuals with unchanged therapy (Con3), similarly to the long-term study with Int52 (n = 39) and Con52 (n = 11). In Int3, fasting serum glucose was reduced by 69+/-47 mg/dl (p < 0.01) compared to baseline and was associated with an increase of Ve from 8.0 +/- 1.6 to 8.8 +/- 1.6 cm/s (p < 0.01) and Vs from 6.2 +/- 1.1 to 6.6 +/- 1.3 cm/s, p < 0.04. In Con3, serum glucose and myocardial velocities were unchanged. In Int52, fasting serum glucose was reduced by 20 +/- 43 mg/dl (p < 0.017) compared to baseline and was associated with an increase of Ve from 7.6 +/- 1.3 to 8.3 +/- 1.7 cm/s (p < 0.002) and a similar trend in Vs (p < 0.07). In Con52, serum glucose and myocardial velocities remained unchanged. Evaluating pooled data, the changes of diastolic myocardial velocity correlated significantly with the changes of serum glucose (r = 0.49, p < 0.004 short- and r = 0.45; p < 0.002 long-term study, respectively). In patients with type 2 diabetes subclinical diastolic myocardial dysfunction, measured as diastolic myocardial velocity by tissue Doppler, improves with better glycemic control.

Comparison of Quetiapine and Risperidone in the Treatment of Schizophrenia

To compare the efficacy and tolerability of quetiapine and risperidone in the treatment of schizophrenia. In this 8-week, double-blind, multicenter, flexible-dose study, patients with schizophrenia (DSM-IV diagnosis) were randomly assigned to quetiapine (200-800 mg/day) or risperidone (2-8 mg/day). The primary hypothesis was that quetiapine was not inferior to risperidone. The primary efficacy measure was change from baseline in Positive and Negative Syndrome Scale (PANSS) total scores; secondary outcomes included response rate (> or = 40% reduction in PANSS scores), Clinical Global Impression-Change (CGI-C), and cognitive and social functioning. Tolerability assessments included treatment-emergent adverse events and changes in weight, glucose, and prolactin. Patients were recruited from June 2001 to September 2002. Patients (N = 673) were randomly assigned to quetiapine (N = 338, mean dose = 525 mg/day) or risperidone (N = 335, mean dose = 5.2 mg/day). The primary analysis demonstrated noninferiority between treatments (p < .05). Improvements with both treatments were comparable on PANSS total, negative, and general psychopathology subscales. Risperidone-treated patients had a significantly (p = .03) greater improvement in PANSS positive subscale score among all patients, but not among completers. Improvements in PANSS response rates, CGI-C, and cognitive function were similar between treatment groups. Changes in serum glucose and weight were minimal and comparable. The rate of extrapyramidal symptom (EPS)-related adverse events was significantly higher with risperidone (22%) than quetiapine (13%; p < .01). Somnolence was more common with quetiapine (26%) than risperidone (20%; p = .04). Prolactin levels increased with risperidone (+35.5 ng/mL), but decreased with quetiapine (-11.5 ng/mL; p < .001). Quetiapine and risperidone had broadly comparable clinical efficacy. Both agents improved cognitive and social functioning, and neither had a clinically significant effect on weight or glucose. Somnolence was more common with quetiapine; EPS and elevated prolactin rates were significantly higher with risperidone.

Equilibrio entre el ejercicio y la insulina: que usted necesita saber

Genetically obese (ob/ob) mice were employed for the study of the effect of metformin on activity and expression of nitric oxide synthase (NOS ) in vitro and in vivo. For in vitro analysis, mouse liver extracts were used. For the in vivo study, (ob/ob) and their control litter mates (ob/c) mice were injected with specified amounts of metformin and the expression of NOS in the adipose tissue and hypothalamus was measured by Western blotting. Results show that metformin exhibited a biphasic effect on NOS activity in vitro. Expression of metformin was differentially altered in the hypothalamus and adipose tissues of the normal and ob/ob animals that were treated with metformin. Further, a significant decrease in food intake occurred in the (ob/ob) mice that received metformin. This decrease in food intake was not accompanied by changes in serum glucose. At inhibitory concentrations, hypothalamic NOS expression changes differentially in normal and ob/ob mice. In normal mice, metformin stimulated NOS expression, while in ob/ob mice there was an inhibition. NOS expression increased in brown adipose tissue of metformin treated control mice, while no such increase was observed in ob/ob mice. No effect of metformin was observed in white adipose tissue of control or obese mice. Thus, metformin may produce anorectic effects through modulation of NOS.

Effect of Divalproex on Metabolic Parameters Is Dose Related in Migraine Prophylaxis

To examine the metabolic effects of three divalproex dosing regimens in patients with migraine. Epidemiological and clinical studies have demonstrated a strong association between serum lipid levels and the development of coronary artery disease. Thus, it is important to understand the impact of chronically administered medications on serum lipids. Metabolic properties of divalproex, an approved and commonly used treatment for migraine prophylaxis, have not been systematically studied in patients with migraine. Adult patients with migraine were randomized to receive one of three daily doses of divalproex (500 mg [n = 45], 1000 mg [n = 43], or 1500 mg [n = 44]) or placebo (n = 44) for 12 weeks. Post hoc analyses were performed to determine the effects of divalproex on total cholesterol, glucose, weight, and body mass index (BMI). The treatment groups were similar at baseline based on demographic and clinical characteristics and the use of concomitant medications. Divalproex resulted in a dose-related mean decrease from baseline in total cholesterol: -5.7 mg/dL or 3% reduction with 500 mg/day; -8.4 mg/dL or 4% reduction with 1000 mg/day; and -12.8 mg/dL or 7% reduction with 1500 mg/day (P < .05 for 1500 mg/day vs. placebo). There were no differences between any divalproex dose group and placebo for mean change from baseline in glucose, weight, or BMI. Divalproex results in a dose-dependent reduction in serum cholesterol within the first 3 months of therapy, with no significant change in serum glucose or BMI.

Hyperglycemia, impaired glucose tolerance and elevated glycated hemoglobin levels in a long-lived mouse stock

We have previously demonstrated that two wild-derived stocks of mice, Idaho and Majuro, are significantly longer-lived than mice of a control stock (DC) generated as a four-way cross of commonly used laboratory strains of mice. This study provides independent confirmation of this earlier finding, as well as examining serum glucose, insulin, leptin, glycated hemoglobin (GHb), cataract severity, and glucose tolerance levels in each of the stocks. Both the mean (+20%) and maximum (+13%) life span of the Idaho mice were significantly increased relative to the DC stock, while in the Majuro mice only maximum (+15%) life span was significantly increased. In addition, Majuro mice were hyperglycemic in both the fed and fasted states compared both to laboratory-derived and Idaho stocks, had significantly elevated GHb levels and cataract scores, and were glucose intolerant although serum insulin levels did not differ between stocks. Body weight and body mass index (BMI)-corrected leptin levels were also dramatically (1.5–3-fold) higher in the Majuro mice. The longevity of Id mice was not accompanied by changes in serum glucose and insulin levels, or glucose tolerance compared to DC controls, although GHb levels were significantly lower in the Idaho mice. Taken together, these findings suggest that neither a reduction of blood glucose levels nor an increase in glucose tolerance is necessary for life span extension in mice.

Effect of Systemic Lupus Erythematosus on some Biochemical Parameters in Female Patients

It has been noticed that there is an increase in the number of women suffering from SLE. Most studies confirmed that serum DHEA (dehydroepiandrosterone) and DHEA sulphate are lower among patients with SLE than among controls even- during phases of inactive disease so we performed this study to detect the level of DHEA-S in the female patients with SLE. The overall results confirm that DHEA treatment was well- tolerated, significantly reduced the number of SLE flares, and improved patient’s global assessment of disease activity. Some serum parameters like liver and kidney functions were detected. Biochemical analysis showed that there is a significant increase of total lipids, cholestrol, triglycerides. But insignificant change in serum glucose, urea nitrogen and uric acid levels were recorded. From the present study three things were concluded. Firstly, there is a strong relationship between level of DHEA and the progression of SLE. Secondly, liver activity and kidney functions were not affected by SLE disease.Thirdly, DHEA treatment has a beneficial effect on female patients. So this study recommended to follow up DHEAS in female patients and use it in a proper dosage. In addition, further study must be done.

Effect of Systemic Lupus Erythematosus on some Biochemical Parameters in Female Patients

It has been noticed that there is an increase in the number of women suffering from SLE. Most studies confirmed that serum DHEA (dehydroepiandrosterone) and DHEA sulphate are lower among patients with SLE than among controls even- during phases of inactive disease so we performed this study to detect the level of DHEA-S in the female patients with SLE. The overall results confirm that DHEA treatment was well- tolerated, significantly reduced the number of SLE flares, and improved patient’s global assessment of disease activity. Some serum parameters like liver and kidney functions were detected. Biochemical analysis showed that there is a significant increase of total lipids, cholestrol, triglycerides. But insignificant change in serum glucose, urea nitrogen and uric acid levels were recorded. From the present study three things were concluded. Firstly, there is a strong relationship between level of DHEA and the progression of SLE. Secondly, liver activity and kidney functions were not affected by SLE disease.Thirdly, DHEA treatment has a beneficial effect on female patients. So this study recommended to follow up DHEAS in female patients and use it in a proper dosage. In addition, further study must be done.

Plasma selenium decrease during pregnancy is associated with glucose intolerance.

There is an increased requirement for selenium during pregnancy, presumably for fetal growth, which manifests as decreasing maternal blood and tissue selenium concentrations. These decreases are greater in pregnant women with gestational or preexisting diabetes. We measured selenium status and glucose tolerance between wk 12 and 34 of gestation in 22 pregnant women. We found that the increase in blood glucose in response to an oral glucose challenge at 12 wk gestation and the increase in fasting glucose during pregnancy were inversely correlated with plasma selenium concentration. Women with lower plasma glutathione peroxidase activities during pregnancy also tended to have higher fasting glucose levels. These inverse relationships between selenium status and glucose tolerance are consistent with earlier observations that suggest a link between selenium and glucose metabolism. The observation that changes in serum glucose were not accompanied by changes in insulin suggests that selenium may affect glucose metabolism downstream from insulin, or through independent energy regulatory pathways such as thyroid hormone.

Serum adiponectin as a biomarker for in vivo PPARgamma activation and PPARgamma agonist-induced efficacy on insulin sensitization/lipid lowering in rats

BackgroundPPARγ agonists ameliorate insulin resistance and dyslipidemia in type 2 diabetic patients. Adiponectin possesses insulin sensitizing properties, and predicts insulin sensitivity of both glucose and lipid metabolism. In diet-induced insulin resistant rats and ZDF rats, the current studies determined the correlation between PPARγ agonist-upregulated fatty acid binding protein(FABP3) mRNA in adipose tissue and PPARγ agonist-elevated serum adiponectin, and the correlation between PPARγ agonist-elevated serum adiponectin and PPARγ agonist-mediated efficacy in insulin sensitization and lipid lowering.ResultsParallel groups of SD rats were fed a high fat/sucrose (HF) diet for 4 weeks. These rats were orally treated for the later 2 weeks with vehicle, either PPARγ agonist GI262570 (0.2–100 mg/kg, Q.D.), or GW347845 (3 mg/kg, B.I.D). Rats on HF diet showed significant increases in postprandial serum triglycerides, free fatty acids (FFA), insulin, and area under curve (AUC) of serum insulin during an oral glucose tolerance test, but showed no change in serum glucose, adiponectin, and glucose AUC. Treatment with GI262570 dose-dependently upregulated adipose FABP3 mRNA, and increased serum adiponectin. There was a positive correlation between adipose FABP3 mRNA and serum adiponectin (r = 0.7350, p < 0.01). GI262570 dose-dependently decreased the diet-induced elevations in triglycerides, FFA, insulin, and insulin AUC. Treatment with GW347845 had similar effects on serum adiponectin and the diet-induced elevations. There were negative correlations for adiponectin versus triglycerides, FFA, insulin, and insulin AUC (For GI262570, r = -0.7486, -0.4581, -0.4379, and -0.3258 respectively, all p < 0.05. For GW347845, r = -0.6370, -0.6877, -0.5512, and -0.3812 respectively, all p < 0.05). In ZDF rats treated with PPARγ agonists pioglitazone (3–30 mg/kg, B.I.D.) or GW347845 (3 mg/kg, B.I.D.), there were also negative correlations for serum adiponectin versus glucose, triglycerides, FFA (for pioglitazone, r = -0.7005, -0.8603, and -0.9288 respectively; for GW347845, r = -0.9721, -0.8483, and -0.9453 respectively, all p < 0.01).ConclusionsThis study demonstrated that (a) PPARγ agonists improved insulin sensitivity and ameliorated dyslipidemia in HF fed rats and ZDF rats, which were correlated with serum adiponectin; (b) Serum adiponectin was positively correlated with adipose FABP3 mRNA in GI262570-treated rats. These data suggest that serum adiponectin can serve as a biomarker for both in vivo PPARγ activation and PPARγ agonist-induced efficacy on insulin resistance and dyslipidemia in rats.

Establishment of a predictive model of serum glucose changes under different exercise intensities and durations among patients with type 2 diabetes mellitus.

Regular exercise is regarded as one of necessary elements in treating diabetes mellitus (DM). The purpose of this study was to investigate the influence of different exercise intensities and durations on serum glucose changes after exercise in type 2 DM patients and to establish a predictive model of changes in serum glucose under different exercise intensities and durations. Thirty-seven type 2 DM patients were recruited from four teaching hospitals. A total of 12 exercise sessions were scheduled according to the results of a graded treadmill exercise test. The 12 exercise sessions were designed on the basis of different exercise intensities (40%, 60%, and 80% maximal workload) and exercise durations (10, 20, 30, and 40 min). Serum glucose level was measured before and after exercise. The findings indicate that the main effect of exercise intensity and duration was significant, but there was no interaction effect. All four variables, including exercise intensity, exercise duration, pre-exercise serum glucose levels, and gender, explained 37% of the variance in serum glucose changes after exercise. In conclusion, a dose-response relationship between exercise amount and serum glucose changes was demonstrated. This is helpful for health professionals to teach type 2 DM patients how to predict serum glucose response in different exercise situations.

Effects of Arm Exercise on Serum Glucose Response in Type 2 DM Patients

The aims of the study were to examine the influence of upper extremity exercise on glucose response and to establish a predictive model of changes in serum glucose under different exercise intensities and durations. Thirty-three type 2 DM patients who met the selection criteria were selected. An arm cycle ergometer exercise test was conducted, and then 12 arm exercise sessions were arranged based on different exercise intensities (40%, 60%, and 80% of maximal workload) and exercise durations (10, 20, 30, and 40 min). Serum glucose levels were measured before and after each exercise session. Serum glucose levels significantly decreased after arm exercise regardless of different intensities or durations. However, no interaction effect (intensity x duration) or main effect in exercise intensity was observed, but a significant main effect in exercise duration was observed (F = 11.756, p <.0001). Also exercise duration was a significant predictor of serum glucose changes after arm exercise. These results suggest that arm exercise can play a useful role in glycemic control for type 2 DM patients and exercise duration is a key factor in determining serum glucose response under upper-extremity exercise.

Serum glucose and lipid changes during the course of clozapine treatment: the effect of concurrent β-adrenergic antagonist treatment

We examined the effects of long-term clozapine treatment, concurrent treatment with β-adrenergic antagonists, and clozapine-induced weight gain on serum glucose and lipid measures. Fifty subjects met the DSM-III-R criteria for schizophrenia or schizoaffective disorder, participated in a 10-week, double-blind comparison of haloperidol and clozapine and a 1-year, open-label clozapine trial, and had available serum glucose and lipid levels. Weight and glucose, and lipid laboratory values were measured at the baseline and throughout the double-blind and year-long study. There were significant increases in serum triglyceride, total cholesterol, and glucose levels during the course of clozapine treatment. There were no significant changes in high-density lipoprotein (HDL) or low-density lipoprotein (LDL). Propranolol and atenolol had additive effects on changes in the total cholesterol and triglycerides, with propranolol having the most pronounced effects. Propranolol and atenolol had no significant effect on the serum glucose levels. There were significant correlations between the triglyceride and HDL level changes and clozapine-associated weight gain during the study. There were no significant correlations between the change in serum total cholesterol, LDL, or glucose and weight gain. Clozapine therapy has adverse effects on glucose and lipid homeostasis, with clozapine-induced changes in serum glucose likely due to the inherent pharmacological properties of clozapine. Concurrent β-adrenergic receptor antagonist treatment may have an additive effect on serum lipids, and clozapine-associated weight gain also plays a modest role in triglyceride increases.

Lipid and exocrine pancreatic ultrastructural changes due to experimental diabetes.

The aim of this study was to establish if the changes in the ultrastructure of the exocrine part of the pancreas are correlated with changes in serum glucose, cholesterol and lipoprotein fractions during the progression of diabetes in rabbits. Diabetes mellitus was induced in male New Zealand rabbits by a single injection of alloxan into the auricular vein. On the day 7th the glucose level in the whole blood was measured and this day was designated as the first day of diabetes. Rabbits were divided into 5 groups: untreated control, 21-day diabetes, 42-day diabetes, 90-day diabetes and 180-day diabetes. The cholesterol, HDL (high-density lipoprotein) and LDL (low-density lipoprotein) levels were examined in the serum. The total pancreatic lipase activity was measured spectrophotometrically in the pancreatic homogenate. Histological specimens were examined under an electron microscopy. The glucose level increased significantly in all of the alloxan exposed animals. The significant elevation of cholesterol level was observed on day 21 and 180. The HDL level was increased (P<0.05) only on the day 21st. The LDL level and the total activity of pancreatic lysosomal lipase increased significantly on day 21, 42 and 90. Further dilation of granular endoplasmic reticular ducts and decrease in the number of zymogen granules were observed amongst exocrine cells. Fragmented mitochondrial and translucent matrix were also seen. Intensification of the pancreatic fibrosis was found on day 90. Microvascular changes were reported in exocrine cells after 180 days. Their nuclei were smaller with large bulges on the nuclear membrane, and the number of heterogeneous electron granules of zymogen further declined. We concluded that the intensification of ultrastructural changes of the exocrine part of the pancreas correlated with the changes of the pancreatic lipase activity, and glucose and lipoprotein levels.

Effect of metformin on nitric oxide synthase in genetically obese (ob/ob) mice

Genetically obese (ob/ob) mice were employed for the study of the effect of metformin on activity and expression of nitric oxide synthase (NOS ) in vitro and in vivo. For in vitro analysis, mouse liver extracts were used. For the in vivo study, (ob/ob) and their control litter mates (ob/c) mice were injected with specified amounts of metformin and the expression of NOS in the adipose tissue and hypothalamus was measured by Western blotting. Results show that metformin exhibited a biphasic effect on NOS activity in vitro. Expression of metformin was differentially altered in the hypothalamus and adipose tissues of the normal and ob/ob animals that were treated with metformin. Further, a significant decrease in food intake occurred in the (ob/ob) mice that received metformin. This decrease in food intake was not accompanied by changes in serum glucose. At inhibitory concentrations, hypothalamic NOS expression changes differentially in normal and ob/ob mice. In normal mice, metformin stimulated NOS expression, while in ob/ob mice there was an inhibition. NOS expression increased in brown adipose tissue of metformin treated control mice, while no such increase was observed in ob/ob mice. No effect of metformin was observed in white adipose tissue of control or obese mice. Thus, metformin may produce anorectic effects through modulation of NOS.

Time course of changes in serum glucose, insulin, lipids and tissue lipase activities in macrosomic offspring of rats with streptozotocin-induced diabetes

Time course of changes in serum glucose, insulin, lipids and tissue lipase activities in macrosomic offspring of rats with streptozotocin-induced diabetes