Effects of a brisk walk on lipoprotein lipase activity and plasma triglyceride concentrations in the fasted and postprandial states

This study aimed to determine whether changes in plasma heparin-releasable lipoprotein lipase (LPL) activity following a brisk walk were associated with decreases in fasting and/or postprandial triglyceride (TG) concentrations. Two groups of pre-menopausal women participated. In one group (fasting study group, n=10), TG concentrations and post-heparin plasma LPL activity were measured in the fasted state on two occasions: ~18 h after a 2-h treadmill walk at 50% maximal oxygen uptake (exercise trial); and after a day of no exercise (control trial). The other group (postprandial study group, n=9) undertook two oral fat tolerance tests (blood samples taken fasting and for 6 h after a high-fat meal), with plasma LPL activity measured 6 h after meal ingestion. Pre-conditions were the same as for the fasting study group (i.e. control and prior exercise). Prior exercise reduced fasting TG concentrations by 23 (7)% (fasting study group) [mean (SEM)] and by 18 (9)% (postprandial study group) (both P<0.05), and the postprandial TG response by 23 (6)% (postprandial study group) (P<0.01). Plasma LPL activity was not significantly increased by exercise in either the fasting or postprandial study groups. However, exercise-induced changes in both fasting and postprandial LPL activity were significantly correlated with the respective exercise-induced changes in fasting TG concentration and the postprandial TG response (r=−0.70 and −0.77 respectively, P<0.05 for both). These data suggest that increased LPL activity may contribute to the hypotriglyceridaemic effect of moderate exercise, although other mechanisms are also likely to be involved. Electronic Publication     

Theophylline disrupts diurnal rhythms of humoral factors with loss of meal cyclicity

To test the possibility that theophylline induced circadian disappearance of food intake might depend upon rhythmic disruption of blood glucose, insulin and free fatty acids (FFA), theophylline was administered chronically. This markedly lengthened postprandial intermeal intervals during the dark, and induced approximately identical intermeal intervals and identical meal sizes in the light and dark periods. In contrast to the clear light-dark dependent oscillations of serum glucose, insulin and FFA in the controls, the theophyllinized rats lost circadian fluctuation of each of these three chemical substances. Further, theophyllinized rats, unlike controls, had no time-dependent fluctuation in the levels of these substances at ? 120, ?60 or ?15 min preceding the onset of the first meal before the dark. These findings, together with previous reports, explain the disappearance of nocturnal feeding rhythm in theophyllinized rats in terms of functional destruction of circadian regulation in the hypothalamus which modulate the production of chemical determinants of food intake.     

Nitric oxide mediates intestinal hyperaemic responses to intraluminal bile-oleate

It has long been recognized that intestinal blood flow increases at mealtimes. Mesenteric hyperaemia is also evoked by activation of sensory peptidergic nerves. Our studies explored the possible role of endogenous nitric oxide (NO) in the rat intestinal vasodilator response to luminal instillation of an oleic acid plus bile mixture before and after acute intrajejunal instillation of capsaicin and after chronic pretreatment with capsaicin. In anaesthetized rats we measured jejunal blood flow (BF) with an ultrasonic Doppler flowmeter and systemic arterial pressure (AP) with a pressure transducer. Intestinal perfusion with 80 mM oleic acid in bile increased BF by 98±12%. Instillation of 4 mg of capsaicin into the jejunal lumen initially increased BF by 42±9% but was followed by vasoconstriction. Inhibition of NO synthase with 25 mg/kg i.v. N-nitro-L-arginine (L-NNA) decreased BF by 27±5% and increased AP by 37±11%. After treatment with L-NNA and after acute and chronic administration of capsaicin, the bile-oleate-induced maximal increases in BF above control levels were 42±7%, 65±12%, and 58±8%, respectively. The observed inhibitory effect of L-NNA on the intestinal hyperaemic response to the bile-oleate mixture was reversed by pretreatment with L-arginine (100 mg/kg i.V.). In capsaicin pretreated rats the subsequent bile-oleate-induced hyperaemia was reduced in magnitude but the inhibitory effects of L-NNA were proportionately the same as in animals not receiving capsaicin. These findings support the hypothesis that NO is involved with bile-oleate-induced mesenteric hyperaemia.     

Acarbose treatments improve arterial stiffness in patients with type 2 diabetes mellitus

Aims/Introduction: Although the improvement of postprandial hyperglycemia by an alpha‐glucosidase inhibitor (α‐GI) has been associated with a risk reduction of cardiovascular events, the relationship between postprandial hyperglycemia and arterial stiffness has not been well understood. We therefore examined whether ameliorating the postprandial state by α‐GI leads to an improvement in arterial stiffness. Materials and Methods: A total of 22 patients with type 2 diabetes mellitus were treated with acarbose. Cardio‐ankle vascular index (CAVI) as the arterial stiffness was measured by using a VaSera CAVI instrument before and 12 months after acarbose treatment. Serum high‐sensitivity C‐reactive protein (hs‐CRP), pentraxin‐3 (PTX3) and matrix metalloproteinase (MMP) ‐2, ‐9 were measured at the same time points. Furthermore, circulating peripheral blood mononuclear cells were examined for the frequencies of CD14 positive cells expressing membrane type‐1 MMP (MT1‐MMP) at the single cell level using flow cytometry. Results: After acarbose treatment, postprandial glucose and glycosylated hemoglobin (HbA_1c) were significantly decreased. Serum levels of hs‐CRP, PTX3, MMP‐2 and MMP‐9 were significantly decreased. CAVI showed a significant reduction, although the changes were not significant in blood pressure and heart rate. MT1‐MMP expression was significantly decreased by acarbose treatment. In multivariate analysis, improvement of blood glucose, decrease of PTX3 levels and MT1‐MMP expression were independent predictors of beneficial change in CAVI. Conclusions: The present study showed that the beneficial effects of acarbose on arterial stiffness are mediated by an improvement of postprandial hyperglycemia and vascular remodeling markers. In conclusion, acarbose treatment might reduce the risk of cardiovascular diseases by altering the arterial stiffness in postprandial hyperglycemic status. (J Diabetes Invest, doi: 10.1111/j.2040‐1124.2010.00079.x , 2010)     

A novel technique of Roux-en-Y gastric bypass reversal for postprandial hyperinsulinemic hypoglycaemia: A case report

BackgroundWe describe an evaluation of the effects of partial Roux-en-Y gastric bypass (RYGB) reversal on postprandial hyperinsulinaemic hypoglycaemia, insulin and GLP-1 levels.Case summaryA 37 year old man was admitted with neuroglycopenia (plasma–glucose 1.6 mmol/l) 18 months after RYGB, with normal 72 h fasting test and abdominal CT. Despite dietary modifications and medical treatment, the hypoglycaemic episodes escalated in frequency. Feeding by a gastrostomy tube positioned in the gastric remnant did not prevent severe episodes of hypoglycaemia. A modified reversal of the RYGB was performed. Mixed meal tests were done perorally (PO), through the gastrostomy tube 1 (GT1), 4 weeks (GT2) after placement and 4 weeks after reversal (POr), with assessment of glucose, insulin and GLP-1 levels.ResultsPlasma–glucose increased to a maximum of 9.6, 5.4, 6.5 and 5.8 mmol/l at the PO, GT1, GT2 and POr tests respectively. The corresponding insulin levels were 2939, 731, 725 and 463 pmol/l. A decrease of plasma–glucose followed: 2.2, 3.0, 3.9 and 2.9 mmol/l respectively and insulin levels were suppressed at 150 min: 45, 22, 21 and 14 pmol/l, respectively. GLP-1 levels increased in the PO test (60 min: 122 pmol/l, 21 fold of basal), but was attenuated in the two latter tests (12–23 pmol/l at 60 min).ConclusionsReduction of plasma–glucose, insulin and GLP-1 excursions and symptoms were seen after gastric tube placement and partial RYGB reversal. This attenuation of GLP-1 response to feeding could reflect an adaptation to nutrients.     

Peripheral arterial disease,type 2 diabetes and postprandial lipidaemia: Is there a link?

Peripheral arterial disease, manifested as intermittent claudication or critical ischaemia, or identified by an ankle/brachial index 0.9, is present in at least one in every four patients with type 2 diabetes mellitus.Several reasons exist for peripheral arterial disease indiabetes. In addition to hyperglycaemia, smoking and hypertension, the dyslipidaemia that accompanies type2 diabetes and is characterised by increased triglyceride levels and reduced high-density lipoprotein cholesterol concentrations also seems to contribute to this association. Recent years have witnessed an increased interest in postprandial lipidaemia, as a result of various prospective studies showing that non-fasting triglycerides predict the onset of arteriosclerotic cardiovascular disease better than fasting measurements do. Additionally,the use of certain specific postprandial particle markers,such as apolipoprotein B-48, makes it easier and more simple to approach the postprandial phenomenon. Despite this, only a few studies have evaluated the role of postprandial triglycerides in the development of peripheral arterial disease and type 2 diabetes. The purpose of this review is to examine the epidemiology and risk factors of peripheral arterial disease in type 2 diabetes, focusing on the role of postprandial triglycerides and particles.     

Postprandial hyperglycemia in type 2 diabetes and obstructive sleep apnea

ObjectivesPostprandial hyperglycemia is common in type 2 diabetes even in those with acceptable glycemic control and conveys an increased risk of cardiovascular morbidity and mortality. Although obstructive sleep apnea (OSA) has been associated with altered glucose metabolism, data regarding its association with postprandial hyperglycemia in type 2 diabetes are limited. Thus, the current study sought to characterize the association between OSA and postprandial hyperglycemia in adults with type 2 diabetes.MethodsA cross-sectional study of adults with type 2 diabetes was conducted. Home sleep testing was used to assess OSA severity as determined by the oxygen desaturation index (ODI). Self-monitoring of blood glucose (SMBG) was performed before and 2-h after breakfast, lunch, and dinner for three days. The association between OSA and glucose levels before and after each meal was examined using multivariable logistic regression.ResultsThe study sample consisted of 195 adults with 52% being men. OSA severity, as assessed by ODI quartiles, was associated with higher postprandial glucose values after dinner but not after breakfast or lunch. The adjusted odds ratios (95% confidence intervals) for a higher post-dinner glucose level for four ODI quartiles were 1.00 (Reference), 2.16 (0.96, 4.87), 2.23 (1.03, 4.83), and 2.58 (1.18, 5.94). Stratified analyses showed that this association was present in men but not women.ConclusionsIncreasing OSA severity is associated with postprandial hyperglycemia in type 2 diabetes and may contribute to impaired glycemic control. Future studies examining the impact of OSA treatment on glucose metabolism should consider meal-related glycemic excursions as a potential outcome.     

The rationale for paired pre- and postprandial self-monitoring of blood glucose: the role of glycemic variability in micro- and macrovascular risk

ABSTRACT

Background: Decisions regarding diabetes management traditionally have been driven by the results of fasting plasma glucose measurement or measurement of glycosylated hemoglobin (A1C), yet glycemic control remains far from optimal in many individuals with diabetes. Mounting evidence implicates glycemic variability, manifested predominantly as postprandial glycemic spikes, as a key factor in the development of macrovascular complications. Recent studies suggest that newer therapies specifically targeting postprandial hyperglycemia can significantly reduce postprandial glucose levels and improve overall glycemic control.

Methods: A Medline search was performed using the term ‘postchallenge’ or ‘postprandial’, together with glucose or diabetes. After excluding review articles and case studies, we reviewed primary articles, meta-analyses, and references therein and selected those that best addressed this topic. Selection bias may be considered a potential limitation of this approach.

Findings: Although not conclusively demonstrated by prospective studies, a wealth of evidence suggests that postprandial hyperglycemia should not be ignored as an important target for preventing complications of diabetes.

Conclusions: Improved detection and management of postprandial hyperglycemia and glycemic variability is necessary to optimize glycemic control. Meal-based self-monitoring of blood glucose (SMBG) has been shown to improve glycemic control as part of a comprehensive management strategy by helping patients understand the effects of food choices, physical activity, and medications on blood glucose concentrations. SMBG can also help healthcare professionals recognize postprandial hyperglycemia, guide therapeutic adjustments and receive more timely feedback regarding medication changes. The arrival of new therapies that specifically target postprandial hyperglycemia offer healthcare professionals the opportunity to optimally manage diabetes.