Plasma Glucose Concentrations In Patients Research Articles

Neokestose suppresses the increase in plasma glucose caused by oral administration of sucrose in a streptozotocin‑induced diabetic rat

Neokestose is considered to have a prebiotic function. However, the physiological activity of neokestose remains unknown. Neokestose has a blastose, a sucrose analog, in its structure. We previously demonstrated that oral administration of blastose to diabetic rats suppressed the increase in plasma glucose (PG) concentration after sucrose administration. Therefore, neokestose might have a similar effect. In this study, we investigated the effects of neokestose on PG concentrations and the mechanism of its action. We first administered neokestose orally to streptozotocin-induced diabetic rats and observed that the expected consequent increase in PG concentration was significantly suppressed. Next, we examined the inhibitory effect of neokestose on glycosidase activity, but observed only a slight inhibitory effect. Therefore, we hypothesized that neokestose might be hydrolyzed by gastric acid to produce blastose. We performed an acid hydrolysis of neokestose using artificial gastric juice. After acid hydrolysis, peaks corresponding to neokestose and its decomposition products including blastose were observed. Therefore, we suggest that neokestose and blastose, a decomposition product, synergistically inhibit glycosidase activity. These findings support the potential use of neokestose as a useful functional oligosaccharide that can help manage plasma glucose concentrations in patients with diabetes mellitus.

Evaluation of Serum 1,5-Anhydroglucitol Levels as Hyperglycemic Indicator in Patients with Newly Diagnosed Type 2 Diabetes Mellitus

Background and Objectives: 1,5-Anhydroglucitol (1,5-AG) is an emerging marker in the acute assessment of glycemia. 1,5-AG has been shown to be associated with glycemic excursions and also been found to have association with microvascular complications of diabetes and atherosclerosis. This study aimed to evaluate serum 1,5-AG concentration in newly diagnosed type 2 diabetes patients and find the correlation between serum 1,5-AG concentration and blood glucose concentration. Materials and Methods: The study group consisted of 60 type 2 diabetes patients aged 35–55 years and 60 age- and sex-matched controls. 1,5-AG plasma level, HbA1c, fructosamine, and blood glucose were measured in all subjects. Data analysis was done using SPSS software. Results and Discussion: 1,5-AG levels were significantly lower in patients with diabetes mellitus when compared with the control group. 1,5-AG serum level negatively correlated with postprandial blood glucose. The linear regression analysis revealed that 1,5-AG had a linear association with postprandial blood glucose. Conclusion: Serum 1,5-AG levels significantly decreased with an increase in plasma glucose concentrations in patients with diabetes mellitus. Thus monitoring of serum 1,5-AG level may be useful for evaluating glycemic control in patients with newly diagnosed diabetes mellitus.

No changes in fasting and 24-hour glucose levels in type 2 diabetic subjects observed after 10 days of L-Isoleucine supplementation

Rationale: Isoleucine (ILE) is known to modulate glucose metabolism, but it remains unclear if daily ILE supplementation is able to lower fasting and 24-hour plasma glucose concentrations in patients with type 2 diabetes (T2D).

The impact of plasma glucose levels on in-hospital and long-term mortality in non-diabetic patients with ST-segment elevation myocardial infarction patients

Objective: Increased admission plasma glucose can be seen in the acute phase of acute coronary syndromes (ACS). Hence, we performed a retrospective study to evaluate the admission plasma glucose concentration in patients with ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (pPCI) and who had no previous diagnosis of Diabetes Mellitus (DM).Method: This retrospective study included 2504 consecutive confirmed STEMI patients treated with pPCI. The patients were divided into quantiles according to the admission glucose levels. Quantile I: 94 ± 7 mg/dL (n= 626), quantile II: 112 ± 5 mg/dL (n = 626), quantile III: 131 ± 6 mg/dL (n= 626), quantile IV: 184 ± 46 mg/dL (n= 626).Results: Patients with higher plasma glucose (Q4) had 6.6 times higher in-hospital all-cause mortality rates (95% CI: 3.95–9.30) and 3.12 times higher (95% CI: 2.2–4.4) long-term all-cause mortality rates than patients with lower plasma glucose (Q1–Q3), who had lower rates and were used as the reference. This significant relationship remained even after adjustment for all confounders. Conclusion: Even though glucose-lowering therapy is recommended in ACS patients with glucose levels >180 mg/dL, our results showed that high plasma glucose, even lower than 180 mg/dL, could predict in-hospital and long-term mortality.

Levels of personality functioning and not depression predict decline of plasma glucose concentration in patients with type 2 diabetes mellitus

AimsPsychosocial variables influence chronic diseases, such as type 2 diabetes mellitus. While there is evidence for a negative impact of depression, much less is known about stable, personality oriented factors. Aim of the study was to assess the impact of depression and personality functioning on glucose regulation in patients with type 2 diabetes. MethodsSeventy-five adult individuals with a first diagnosis of type 2 diabetes were consecutively recruited in an outpatient medical practice. Plasma glucose (HbA1c) was measured at initial contact, and after three and six months of a standardized disease management program. Depression was assessed by self-report (Patient Health Questionnaire, PHQ-D), levels of personality functioning with the screening version of the Operationalized Psychodynamic Diagnosis structure questionnaire (OPD-SQS). ResultsUsing mixed regression models, OPD-SQS scores were associated with lower baseline levels of HbA1c, but a less steep decline over time. PHQ-D scores were neither associated with intercept nor with slopes of HbA1c. ConclusionsIn type 2 diabetes, levels of personality functioning but not depression predicted decline in plasma glucose during the first six months of a standardized disease management program. Personality functioning may be especially important in chronic diseases that demand a high level of compliance and lifestyle change.

Glucose-lowering effects and mechanisms of the bile acid-sequestering resin sevelamer.

Sevelamer, a non-absorbable amine-based resin used for treatment of hyperphosphataemia, has been demonstrated to have a marked bile acid-binding potential alongside beneficial effects on lipid and glucose metabolism. The aim of this study was to investigate the glucose-lowering effect and mechanism(s) of sevelamer in patients with type 2 diabetes. In this double-blinded randomized controlled trial, we randomized 30 patients with type 2 diabetes to sevelamer (n = 20) or placebo (n = 10). Participants were subjected to standardized 4-hour liquid meal tests at baseline and after 7 days of treatment. The main outcome measure was plasma glucagon-like peptide-1 excursions as measured by area under the curve. In addition, blood was sampled for measurements of glucose, lipids, glucose-dependent insulinotropic polypeptide, C-peptide, glucagon, fibroblast growth factor-19, cholecystokinin and bile acids. Assessments of gastric emptying, resting energy expenditure and gut microbiota composition were performed. Sevelamer elicited a significant placebo-corrected reduction in plasma glucose with concomitant reduced fibroblast growth factor-19 concentrations, increased de novo synthesis of bile acids, a shift towards a more hydrophilic bile acid pool and increased lipogenesis. No glucagon-like peptide-1-mediated effects on insulin, glucagon or gastric emptying were evident, which points to a limited contribution of this incretin hormone to the glucose-lowering effect of sevelamer. Furthermore, no sevelamer-mediated effects on gut microbiota composition or resting energy expenditure were observed. Sevelamer reduced plasma glucose concentrations in patients with type 2 diabetes by mechanisms that seemed to involve decreased intestinal and hepatic bile acid-mediated farnesoid X receptor activation.

Evaluating the Role of Serum 1,5-Anhydroglucitol Concentrations as an Indicator of Hyperglycemic Changes in Diabetic and Non Diabetic Surgical Patients

Purpose: We investigated the relationship between plasma glucose and serum 1,5-anhydroglucitol (1,5-AG) concentrations in surgical patients to determine the role of 1,5-AG concentrations in perioperative glycemic control. Methods: We enrolled 57 patients (19 with and 38 without diabetes) in the study, who underwent hepatectomy under general anesthesia with sevoflurane and remifentanil. Plasma glucose and serum 1,5-AG concentrations were measured and their correlations were evaluated. Results: In all patients, plasma glucose concentrations increased significantly during hepatectomy, but serum 1,5-AG concentrations declined after surgery. Linear regression analysis revealed a weak but significant correlation between the decrease rate of 1,5-AG concentrations and the increase rate of plasma glucose concentrations. Regression analyses revealed this correlation to be more intense in patients without diabetes than in all patients, whereas no correlation was observed in patients with diabetes. These results suggest that serum 1,5- AG concentrations decrease significantly in proportion to increase in plasma glucose concentrations in patients without diabetes, but are less sensitive to such changes in patients with diabetes. Consequently, this indicates that preoperative serum 1,5-AG concentrations in patients with diabetes are too low to be influenced by glycemic fluctuations. In both patient groups, decreased 1,5-AG concentrations did not normalize until 72 h after initiation of surgery. Conclusion: Measurement of 1,5-AG concentrations may be a useful for evaluating glycemic control during anesthesia in patients with normal glycemic metabolism; however, this approach may not be as useful in patients with diabetes as in those without diabetes.

The feature, diagnosis, and treatment of fulminant type 1 diabetes

Type 1 diabetes includes two categories:autoimmune (type 1A) and idiopathic (type 1B)diabetes.Fulminant type 1 diabetes is a recently discovered subtype of type 1 diabetes with extremely rapid progression of hyperglycemia and ketoacidosis.The prevalence of fulminant type 1 diabetes among acute-onset type1 diabetic patients is around 15%-20%.Class Ⅱ HLA genotype and virus infection may contribute to its development.The near-normal HbA_(1C) level despite a very high plasma glucose concentration in patients with ketoacidosis is the clue to diagnosis of fulminant type 1 diabetes.Treatment must be started immediately and aggressively when the diagnosis of fulminant type 1 diabetes is made or strongly suspected. Key words: Diabetes mellitus,type 1; Fulminant diabetes mellitus; Diagnosis; Therapy

Plasma glucose level in Nigerian Africans with head injury

Trauma is often associated with increased plasma glucose concentrations. This prospective study was designed to determine random plasma glucose concentrations in patients with head injury in our center and to determine if this is related to injury severity and outcome. Patients with head injury in whom the plasma glucose concentration could be determined at our accident and emergency unit during the study period were included. We obtained information on demographic data, diagnosis, injury severity using Glasgow Coma Scale scores, treatment with glucose-containing fluid prior to presentation in our center, plasma glucose on admission, 24 hours later and 72 hours later and outcome at discharge using the Glasgow Outcome Scale score. Hyperglycemia was defined as glucose concentrations above 11.1 mmol/L. Fifty eight patients were included in the study from October 2004 to December 2005. There were 46 males and 12 females (4:1). The mean age (± standard deviation [SD]) was 31.3 (16.4) years. Fourteen patients (24.1%) had mild head injury, 21 patients (36.2%) had moderate head injury and 23 patients (39.7%) had severe head injury. The outcome was good in 29 patients (50%), moderate disability in five patients (8.6%), severe disability in one (1.7%) and death in 10 (17.2%). Eighty percent of the patients who died had severe head injury. Most of the patients had a plasma glucose in the normal range irrespective of the severity of the head injury. Only one patient had a plasma glucose in the hyperglycemic range and that patient had a severe head injury. Fifty percent of the patients who died had a plasma glucose concentration in the normal range; none in the hyperglycemic range. This study shows that the plasma glucose is generally below hyperglycemic concentration in our patients irrespective of the severity of head injury.

The effects of propofol, desflurane and isoflurane on plasma glucose concentrations in patients undergoing intracranial mass operation

The effects of propofol, desflurane and isoflurane on plasma glucose concentrations in patients undergoing intracranial mass operation

Skeletal muscle magnesium content is correlated with plasma glucose concentration in patients with essential hypertension treated with lisinopril or bendrofluazide

The association between change in glucose metabolism and change in skeletal muscle magnesium (Mg) concentration induced by antihypertensive treatment was evaluated in 37 patients with essential hypertension randomly treated with either lisinopril or bendrofluazide. Before and after 6 months of treatment, skeletal muscle biopsies were performed, glucose tolerance was determined by oral (OGTT) and intravenous glucose tolerance tests (IVGTT), and insulin sensitivity was assessed by the hyperinsulinemic euglycemic clamp technique. An inverse relationship was found between the treatment-induced change in fasting plasma glucose concentration and change in skeletal muscle Mg concentration (r = −0.39, P < .05). However, there was no significant correlation between skeletal muscle Mg content and either insulin sensitivity measured by the hyperinsulinemic euglycemic clamp test or glucose tolerance evaluated by IVGTT and OGTT. In conclusion, an increased circulating glucose concentration was correlated with a decreased Mg concentration in skeletal muscle during antihypertensive treatment. However, the Mg concentration in skeletal muscle did not significantly predict the insulin sensitivity or glucose tolerance.

Angiotensinogen gene polymorphism is associated with insulin resistance in nondiabetic men with or without coronary heart disease

Background Variants of the angiotensinogen gene may increase the risk of having arterial hypertension and coronary heart disease (CHD), but their effect on insulin resistance remains unknown. Methods We determined M235 and T174 allele status and fasting plasma glucose, insulin, and lipids values in nondiabetic men with CHD documented on angiography ( n = 102) and in a control group ( n = 145). Plasma glucose and insulin responses to 75 gm oral glucose tolerant test and insulin resistance as measured by an insulin suppression test were also carried out in 46 (45%) patients with CHD and in 73 (50%) members of a control group. Results We found no association between M235T status and blood pressure, fasting plasma glucose, insulin, most of the lipids values, and insulin resistance in patients with CHD and normal subjects. Nevertheless, compared with individuals with homozygotes T174, subjects with heterozygotes T174M were associated with greater glucose and insulin response to the oral glucose tolerance test and insulin resistance indicated by higher steady state plasma glucose concentrations in patients with CHD (14.7 ± 0.9 vs 11.3 ± 0.7 mmol/L, p < 0.04). Similar findings were found in the control group, with higher steady-state plasma glucose values in individuals with heterozygotes T174M than in those with homozygotes T174 (10.1 ± 1.4 vs 7.7 ± 0.4 mmol/L, p < 0.05). Conclusion We suggest that the angiotensinogen T174M allele might be associated with insulin resistance in nondiabetic men with and without CHD. (Am Heart J 1998;136:125-31.)

Postprandial glucose and vascular disease.

The high plasma glucose concentrations in patients with diabetes are associated with an increased risk of vascular disease. In patients with non-insulin-dependent diabetes mellitus, vascular changes often predate clinical diagnosis of hyperglycaemia. Impaired glucose tolerance precedes diabetes and may therefore be an important phase in the development of vascular changes. There is evidence to suggest that hyperglycaemia interferes with the activity and function of endothelial cells. In vitro data show that high glucose concentrations can activate protein kinase C (PKC) in endothelial cells, specifically PKC alpha. This activation appears to stimulate expression of adhesion molecules on endothelial cells, facilitating the adhesion and uptake of leukocytes into the endothelium. In addition, high glucose concentrations affect the permeability of tight junctions between endothelial cells, which also seems to be mediated by PKC. Thus, PKC activation may be central to the effects of glucose-stimulated vascular changes. Evidence for direct stimulation of endothelial cells by glucose may support the hypothesis that postprandial glucose spikes are important in the early development of micro- and macrovascular disease.

Hyperproinsulinaemia and islet dysfunction in the NIDDM-like syndrome of Psammomys obesus.

Patients with Type 2, non-insulin dependent diabetes (NIDDM) exhibit elevated plasma proinsulin to insulin ratios [1–9]. Recently, it has been shown that the plasma proinsulin-like fraction in these patients as well as in normal individuals is comprised of both proinsulin and partially cleaved proinsulin, primarily des 31, 32 proinsulin [7,8]. It is assumed that the elevated ratio between proinsulin-related peptides and insulin reflects a β-cell abnormality, since the metabolic clearance rate of these peptides does not differ appreciably between normal individuals and patients with diabetes [10]. Reduction of the plasma glucose concentration in patients with NIDDM, irrespective of the means, was shown to improve insulin production and reduce the degree of hyperproinsulinaemia [3, 11–15]. These observations in man, as well as studies in animal models of diabetes [16–23] have led to the notion that hyperglycaemia per se might be implicated in the generation of a defective β-cell secretory response [24]. Alternatively, hyperglycaemia may play an important contributory role by amplifying a genetically determined β-cell defect, which may not be apparent until unmasked by a chronic increase in secretory demand.

Relationship between hepatic glucose production and fasting plasma glucose concentration in patients with NIDDM

Relationship between hepatic glucose production and fasting plasma glucose concentration in patients with NIDDM

Higher glycemic thresholds for symptoms during beta-adrenergic blockade in IDDM.

We tested the hypotheses that nonselective beta-adrenergic blockade does not cause absolute hypoglycemia unawareness but shifts the glycemic thresholds for symptoms to lower plasma glucose concentrations and that neither neuroglycopenic symptoms nor cognitive impairments during hypoglycemia are altered by beta-adrenergic blockade. To do so, we applied the euglycemic and stepped hypoglycemic clamp techniques to patients with moderately controlled insulin-dependent diabetes mellitus (IDDM) in the absence (n = 8) and presence (n = 9) of the nonselective beta-adrenergic antagonist propranolol. Compared with the corresponding euglycemic clamps, total symptom scores first increased at the 4.4-mM plasma glucose step (a higher level than that of 2.8 mM in nondiabetic subjects studied previously) in the absence of propranolol. Beta-adrenergic blockade did not produce absolute hypoglycemia unawareness. Indeed, at the frankly hypoglycemic step of 2.8 mM, total symptom scores tended to be higher in the presence than in the absence of propranolol. This was largely the result of greater (P less than 0.01) perception of diaphoresis. However, symptom scores did not increase until the 3.3-mM plasma glucose step during beta-adrenergic blockade. The perception of hunger, and perhaps that of tremulousness, was reduced by propranolol at the higher glucose steps. Neuroglycopenic symptoms were not reduced by propranolol. The cognitive function of memory, but not that of attention, was impaired, also starting at the 4.4-mM glucose step. This was not impaired further by propranolol. Thus, we formed the following conclusions. 1) Nonselective beta-adrenergic blockade does not cause absolute hypoglycemia unawareness but shifts the glycemic thresholds for symptoms to lower plasma glucose concentrations in patients with IDDM. 2) Beta-adrenergic blockade does not reduce neuroglycopenic symptoms, and it does not further impair cognitive function during hypoglycemia in IDDM patients.

How Does Glibenclamide Lower Plasma Glucose Concentration in Patients with Type 2 Diabetes?

Twelve patients with Type 2 diabetes and uncontrolled hyperglycaemia, never before treated with anti-diabetic drugs, were studied before and after several months of glibenclamide therapy. Fasting plasma glucose fell significantly (p less than 0.01) from 12.5 +/- 1.1 (mean +/- SE) to 8.3 +/- 0.4 mmol l-1 with glibenclamide therapy, as did glycosylated haemoglobin (from 12.0 +/- 0.9 to 8.4 +/- 0.7%). The improvement in blood glucose control was accompanied by an increase in postprandial plasma insulin concentration measured hourly from 0800 to 1600 h (p less than 0.001). Over the same period, plasma NEFA and lactate levels were significantly (p less than 0.001) lower after treatment with glibenclamide. Mean (+/- SE) insulin-mediated glucose metabolic clearance rate was evaluated during glucose clamp studies, and was significantly higher (p less than 0.001) after glibenclamide therapy at steady-state insulin levels of approximately 10 mU l-1 (53 +/- 3 vs 38 +/- 2 ml-2 min-1) and approximately 70 mU l-1 (78 +/- 9 vs 55 +/- 6 ml m-2 min-1). Hepatic glucose production was also lower following glibenclamide treatment at both the lower (56 +/- 5 vs 68 +/- 5 mg m-2 min-1) and higher 22 +/- 4 vs 32 +/- 6 mg m-2 min-1) insulin levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of sulfonylurea therapy and plasma glucose levels on hemoglobin A1c in type II diabetes mellitus

It is well known that hemoglobin A1c reflects plasma glucose concentrations in patients with diabetes mellitus. To examine hemoglobin A1c and plasma glucose relationships in sulfonylurea-treated patients, 25 patients with well-controlled type II diabetes (fasting plasma glucose 128 ± 6 mg/dl, hemoglobin A1c 7.6 ± 0.5 percent) were evaluated in a double-blind study. This study was divided into two phases (periods I and II). During period I each patient was given a diet plus a placebo and was followed every two weeks until the mean of two consecutive plasma glucose determinations was more than 50 mg/dl above the initial plasma glucose concentration obtained while the patient was taking sulfonylurea. At that point each patient entered period II. At the beginning of period II each patient was switched in a double-blind fashion to either diet plus a placebo or diet plus tolazamide. Fasting plasma glucose concentrations increased to 178 ± 9 mg/dl (p < 0.005) for all patients by week 2 of period I. The increase in hemoglobin A1c concentration was seen to lag behind the increasing fasting plasma glucose concentration by four to six weeks. Fasting plasma glucose and hemoglobin A1c concentrations returned to values indistinguishable from initial values in patients who were given tolazamide and who responded to it. A positive correlation was noted when the hemoglobin A1c concentration was compared with the fasting plasma glucose concentration measured four to six weeks previously.