Inter-relationships between gastric emptying and glycaemia:Implications for clinical practice

Gastric emptying(GE)exhibits a wide inter-individual variation and is a major determinant of postprandial glycaemia in health and diabetes;the rise in blood glucose following oral carbohydrate is greater when GE is relatively more rapid and more sustained when glucose tolerance is impaired.Conversely,GE is influenced by the acute glycaemic environment acute hyperglycaemia slows,while acute hypoglycaemia accelerates it.Delayed GE(gastroparesis)occurs frequently in diabetes and critical illness.In diabetes,this poses challenges for management,particularly in hospitalised individuals and/or those using insulin.In critical illness it compromises the delivery of nutrition and increases the risk of regurgitation and aspiration with consequent lung dysfunction and ventilator dependence.Substantial advances in knowledge relating to GE,which is now recognised as a major determinant of the magnitude of the rise in blood glucose after a meal in both health and diabetes and,the impact of acute glycaemic environment on the rate of GE have been made and the use of gut-based therapies such as glucagon-like peptide-1 receptor agonists,which may profoundly impact GE,in the management of type 2 diabetes,has become commonplace.This necessitates an increased understanding of the complex inter-relationships of GE with glycaemia,its implications in hospitalised patients and the relevance of dysglycaemia and its management,particularly in critical illness.Current approaches to management of gastroparesis to achieve more personalised diabetes care,relevant to clinical practice,is detailed.Further studies focusing on the interactions of medications affecting GE and the glycaemic environment in hospitalised patients,are required.

Gastric emptying, postprandial blood pressure, glycaemia and splanchnic flow in Parkinson's disease

AIM: To determine gastric emptying, blood pressure, mesenteric artery blood flow, and blood glucose responses to oral glucose in Parkinson's disease. METHODS: Twenty-one subjects(13 M, 8 F; age 64.2 ± 1.6 years) with mild to moderate Parkinson's disease(Hoehn and Yahr score 1.4 ± 0.1, duration of known disease 6.3 ± 0.9 years) consumed a 75 g glucose drink, labelled with 20 MBq 99mTc-calcium phytate. Gastric emptying was quantified with scintigraphy, blood pressure and heart rate with an automated device, superior mesenteric artery blood flow by Doppler ultrasonography and blood glucose byglucometer for 180 min. Autonomic nerve function was evaluated with cardiovascular reflex tests and upper gastrointestinal symptoms by questionnaire. RESULTS: The mean gastric half-emptying time was 106 ± 9.1 min, gastric emptying was abnormally delayed in 3 subjects(14%). Systolic and diastolic blood pressure fell(P < 0.001) and mesenteric blood flow and blood glucose(P < 0.001 for both) increased, following the drink. Three subjects(14%) had definite autonomic neuropathy and 8(38%) had postprandial hypotension. There were no significant relationships between changes in blood pressure, heart rate or mesenteric artery blood flow with gastric emptying. Gastric emptying was related to the score for autonomic nerve function(R = 0.55, P < 0.01). There was an inverse relationship between the blood glucose at t = 30 min(R =-0.52, P < 0.05), while the blood glucose at t = 180 min was related directly(R = 0.49, P < 0.05), with gastric emptying. CONCLUSION: In mild to moderate Parkinson's disease, gastric emptying is related to autonomic dysfunction and a determinant of the glycaemic response to oral glucose.

Upper gastrointestinal function and glycemic control in diabetes mellitus

Recent evidence has highlighted the impact of glycemic control on the incidence and progression of diabetic micro- and macrovascular complications, and on cardiovascular risk in the non-diabetic population. Postprandial blood glucose concentrations make a major contribution to overall glycemic control, and are determined in part by upper gastrointestinal function. Conversely, poor glycemic control has an acute, reversible effect on gastrointestinal motility. Insights into the mechanisms by which the gut contributes to glycemia have given rise to a number of novel dietary and pharmacological strategies designed to lower postprandial blood glucose concentrations.

Nutrient stimulation of mesenteric blood flow-implications for older critically ill patients

Nutrient ingestion induces a substantial increase in mesenteric blood flow. In older persons(aged ≥ 65 years), particularly those with chronic medical conditions, the cardiovascular compensatory response may be inadequate to maintain systemic blood pressure during mesenteric blood pooling, leading to postprandial hypotension. In older ambulatory persons, postprandial hypotension is an important pathophysiological condition associated with an increased propensity for syncope, falls, coronary vascular events, stroke and death. In older critically ill patients, the administration of enteral nutrition acutely increases mesenteric blood flow, but whether this pathophysiological response is protective, or precipitates mesenteric ischaemia, is unknown. There are an increasing number of older patients surviving admission to intensive care units, who are likely to be at increased risk of postprandial hypotension, both during, and after, their stay in hospital. In this review, we describe the prevalence, impact and mechanisms of postprandial hypotension in older people and provide an overview of the impact of postprandial hypotension on feeding prescriptions in older critically ill patients. Finally, we provide evidence that postprandial hypotension is likely to be an unrecognised problem in older survivors of critical illness and discuss potential options for management.

Management of critically ill patients with type 2 diabetes:The need for personalised therapy

Critical illness in patients with pre-existing diabetes frequently causes deterioration in glycaemic control.Despite the prevalence of diabetes in patients admitted to hospital and intensive care units,the ideal management of hyperglycaemia in these groups is uncertain.There are data that suggest that acute hyperglycaemia in critically ill patients without diabetes is associated with increased mortality and morbidity.Exogenous insulin to keep blood glucose concentrations < 10 mmol/L is accepted as standard of care in this group.However,preliminary data have recently been reported that suggest that chronic hyperglycaemia may result in conditioning,which protects these patients against damage mediated by acute hyperglycaemia.Furthermore,acute glucose-lowering to < 10 mmol/L in patients with diabetes with inadequate glycaemic control prior to their critical illness appears to have the capacity to cause harm.This review focuses on glycaemic control in critically ill patients with type 2 diabetes,the potential for harm from glucose-lowering and the rationale for personalised therapy.

Development of innovative tools for investigation of nutrient-gut interaction

The gastrointestinal tract is the key interface between the ingesta and the human body.There is wide recognition that the gastrointestinal response to nutrients or bioactive compounds,particularly the secretion of numerous hormones,is critical to the regulation of appetite,body weight and blood glucose.This concept has led to an increasing focus on“gut-based”strategies for the management of metabolic disorders,including type 2 diabetes and obesity.Understanding the underlying mechanisms and downstream effects of nutrient-gut interactions is fundamental to effective translation of this knowledge to clinical practice.To this end,an array of research tools and platforms have been developed to better understand the mechanisms of gut hormone secretion from enteroendocrine cells.This review discusses the evolution of in vitro and in vivo models and the integration of innovative techniques that will ultimately enable the development of novel therapies for metabolic diseases.