How To Control Postprandial Blood Sugar
How To Control Postprandial Blood Sugar – Postprandial glycemic control is an important goal of optimal management of type 2 diabetes, but is often difficult to achieve. The gastrointestinal tract plays a major role in regulating postprandial glycemia in health and diabetes. Various strategies have been proposed to improve gut function, mainly through delaying gastric emptying and/or stimulation of the incretin hormone GLP-1, which are summarized in this review.
The importance of glycemic control in the proper management of diabetes is now well established (1). Glycemic control can be assessed in a number of ways, including resting blood glucose, fasting glucose, postprandial glucose, oral glucose tolerance test or OGTT [which includes fasting glucose and the glycemic response to an oral glucose load (usually 75 g)] and glycated. hemoglobin or HbA1c (which shows overall glycemia over 8-12 weeks). Traditionally, OGTT has been considered the gold standard test for diabetes diagnosis, although HbA1c is still widely used. Fast glucose is widely used in the diagnosis and diagnosis of type 2 diabetes. In contrast, postprandial glycemia has received very little attention, although its importance in glycemia in general in type 2 diabetes is recognized, with potential importance as an independent risk factor for macrovascular disease (2). Postprandial hyperglycemia is often the first symptom of glucose intolerance (3). Impaired glucose tolerance, defined as an abnormal PPG (7.8–11.1 mmol) in the presence of normal fasting glucose, i.e., particularly abnormal postprandial glycemic levels, is considered prediabetes, which can lead to type 2 diabetes. . In type 2 diabetes, PPG contributes significantly to overall glycemia as measured by HbA1c and is a major contributor (ie, >50%) when the latter is ≤8.0% (4, 5). The importance of targeting PPG to achieve desired glycemic goals has been increasingly recognized over the past two decades. In 2001, the ADA published a consensus statement on PPG, and then, in 2014, the International Diabetes Federation (IDF) issued specific guidelines for the management of type 1 PPG and type 2 diabetes, advocating dietary strategies (such as low-glycemic index foods) and antidiabetic use of drugs (eg, GLP-1 agonists) that cause postprandial glycemia (2, 6). Postprandial hyperglycemia is not only associated with microvascular disease, but may increase the risk of cardiovascular complications. The DECODE study reported that PPG was a better predictor of all-cause mortality and cardiovascular disease in type 2 diabetes than fasting plasma glucose (FPG) (7).
How To Control Postprandial Blood Sugar
Several factors affect postprandial glycemia. Although these include preprandial glycemia, insulin secretion and sensitivity (hepatic and skeletal secretion), and glucagon secretion, this review focuses on gastrointestinal factors, particularly gastric emptying and gastric carbohydrate absorption. , and incretin gastric inhibitory polypeptide or glucose-polypeptide insulinotropic hormones. ) and glucagon-like peptide 1 (GLP-1) (6). The importance of the gastrointestinal tract in modulating postprandial glycemia depends on the level of glucose tolerance. Another way to estimate this contribution is to calculate the so-called GIGD of gastrointestinal glucose disposal; the amount of intravenous sugar needed to “copy” the sugar after the sugar is in the mouth – If 25 g of sugar are needed to copy 75 g of oral sugar, the GIGD reaches 100 × (75 – 25 )/75 = 66% (8 , 9). In other words, in this case, the digestive tract can get rid of 50 g of sugar. In good health, GIGD is about 66%. However, in type 2 diabetes, GIGD is greatly reduced and may even be zero (10). Recent studies have provided important insight into the importance of abortion and incretin hormones in GIGD.
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Gastric emptying is a physiological process by which nutrients are transferred from the stomach to the duodenum at a strictly controlled rate to improve digestion and absorption (11). Gastric emptying is a complex coordinated process involving gastric smooth muscle, neural network (Auerbach’s and Meissner’s plexus), vagal and enteric nervous systems, neurotransmitters such as nitric oxide, cells of the immune system, and gastric pacemaker cells. known as an interstitial. Cells of Cajal (ICC) (11). Ingested solid food is first stored in the stomach as it is ground into small particles, usually less than 1 mm in size. This process is called trituration. Food particles are passed through the pylorus into the duodenum, mainly during perforation. The overall rate of gastric emptying depends on food composition and macronutrient quality (12). Liquids drain in a special way compared to solids. Difficult urination usually has a delay of about 20 minutes, while liquid drinks are immediately empty. After the sliding phase of gastric emptying of nutrient-rich foods (solid or liquid), they are usually sought in a generally linear fashion over time, whereas the excretion of non-nutritive liquids follows a non-stationary, non-dependent, mono-exponential pattern. Consequently, the amount of food consumed does not significantly affect the rate of excretion of nutrients, not the time. In healthy people, the output from the stomach varies from person to person (about 1-3 kcal/min), but the reduction is great for every person (13). Abnormally delayed gastric emptying, or gastroparesis, is often present in diabetes. Various studies show that 30-50% of patients with long-term complicated type 1 or type 2 diabetes have gastroparesis. A characteristic feature of cellular gastroparesis is the loss of ICC (14). On the other hand, gastric emptying can be accelerated in some diabetics, especially people with uncomplicated type 2 diabetes (15) and young people with type 2 diabetes 1 (16). Therefore, the individual variability of excretion in diabetes is even greater than in health. It is important to predict the rate of rejection, whether normal, slow, or rapid, for a given individual based on clinical criteria. Upper gastrointestinal symptoms, including postprandial hunger, nausea, vomiting, bloating, upper abdominal pain, and early satiety (17) are common in diabetes (18) and patients with gastroparesis often have upper gastrointestinal symptoms, the association between symptom occurrence and gastroparesis is most straightforward.
Intestinal excretion is the main cause of postprandial glycemic excursions in health and diabetes, accounting for a third of the difference in the initial rise in glucose. The association of gastric emptying rate with PPG depends on time and level of glucose tolerance (19). Therefore, in good health, an oral glucose load follows.
The progression of plasma glucose (30 or 60 minutes) is directly related to the discharge rate, while the diagnostic value of 120 minutes has a different relationship, but in people with sugar intolerance or type 2. In diabetes, the ratio shows a shift “to the right,” so that a direct relationship is seen even after 60 minutes (19, 20).
Scintigraphy is the “gold standard” method for measuring gastric emptying and allows accurate measurement of solid and liquid excretion simultaneously. The American Neurogastroenterology and Motility Society and the Society of Nuclear Medicine have proposed an experimental diet consisting of two large eggs, two slices of bread and strawberry jam (30 g) in water (120 ml) containing 255 kcal (composition). 72% carbohydrates, 24% protein, 2% fat and 2% fiber). Foods are radiolabeled with 1mCi 99Tc sulfur colloid (21). These foods may be suitable for a Western diet, but their universal applicability is questionable. The limitations of scintigraphy are related to radiation and the need for specialized nuclear medicine equipment and trained personnel. One of the best methods is stable isotope analysis of breath, which, although a measure of perception rather than accuracy, correlates well with scintigraphy and is a noninvasive method without radiation. Subjects eat foods containing a
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In the liver and out of the lungs. Breath samples are taken 2-4 hours after a meal. Ultrasound can also be used to measure discharge, but is observer dependent and requires highly trained personnel. In clinical trials, one of the most common methods of measuring gastric emptying is to use the plasma kinetics of oral paracetamol absorption. Although inexpensive and simple, it is an imprecise method that cannot be used to assess gastric emptying and is not recommended (22). Single-photon emission computed tomography (SPECT), magnetic resonance imaging (MRI) and 3D ultrasound are also non-invasive methods capable of providing true 3D images of the effect of food on gastric volume and gastric accommodation, but remain research methods.
Since the 1960s, it has been known that blood glucose levels are significantly lower after oral administration compared with similar intravenous glucose control (23). This indicates a significant increase in insulin production after oral glucose administration, a phenomenon known as the “incretin effect” (24). In the late 1980s, the factors responsible for incretin action, the so-called “incretin” hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1) were discovered (25). GIP and GLP-1 are gut-derived peptides produced from entero-endocrine K (mainly in the small intestine) and L (mainly in the large intestine), respectively. All nutrients have the ability to stimulate the secretion of incretin hormones, although their relative strength varies (fats and proteins can be stronger triggers of incretin release than carbohydrates). Although fasting levels are low, plasma levels of GLP-1 and GIP rise immediately after a meal (26). Circulating GLP-1 and GIP are rapidly degraded by the ubiquitous enzyme dipeptidyl peptidase-IV (DPP-IV) and renal clearance, so their half-lives are only.
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