Diabetic gastroparesis diet

Richard Bernstein: Dr Bernstein's Diabetes Solution

An orchestrated function of all these components is required for the appropriate propulsive movement of the food in the gastrointestinal tract. Gastroparesis, a pathological slowing-down of gastric emptying, is a result of the damage to the tissue elements involved in the regulation of motility.

Gastroparesis is one of the well-known complications of longstanding diabetes mellitus. Although it is rarely a lifethreatening complication, it has a deteriorating effect on the quality of life, leads to unpredictable oscillation of the blood glucose level, and increases the time required for the absorption of food and medicines.

This review describes the clinical characteristics of diabetic gastroparesis and summarizes the organic and functional motility abnormalities caused by diabetic gastroparesis diet This article is part of the Topical Collection on Microvascular Complications—Neuropathy V. Kempler e-mail: kempler. Lengyel : T. Várkonyi 1st. Lengyel e-mail: lecs in1st. Várkonyi e-mail: varkonyitamas gmail.

Finally, the currently available and potential future therapeutic approaches are summarized.

Gastroparesis Diet Guidelines

Keywords Diabetes mellitus. Interstitial cells of Cajal. Neural elements.

Richard Bernstein: Dr Bernstein's Diabetes Solution

Furthermore, a normal gastric motility rate does not exclude the possibility that the complaints originate from motility disorders, while a slower gastric motility is not always associated with symptoms [11]. It is important to emphasize that the only manifestation of gastroparesis in some patients without GI symptoms is poor glycemic control, whereas in other cases, diabetic gastroparesis diet completely opposite phenomenon may be experienced: the presence of obvious symptoms are not related to dysglycemia [12].

Due to delayed food absorption, postprandial hypoglycemia might be a characteristic feature of gastroparesis among insulin-treated diabetic patients. Although slower stomach emptying in a case of long-standing diabetes mellitus rarely leads to life-threatening complications and does not increase mortality [13], it increases the risk of an diabetic gastroparesis diet imbalance, as well as hypo- or hyperglycemia. Gastroparesis should also be considered as the underlying mechanism among patients thought to have brittle diabetes.

As diabetic gastroparesis diet various other areas of medicine, the severity of the disease may be characterized by different scoring systems.

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Further investigations are required to test whether these questionnaires are sufficiently valuable to guide the proper therapeutic approach or how well these scores lead to an estimate of the prognosis of the gastric complication. The mixing and the propulsive movement of liquid and solid food arriving into the esophagus and the lower parts of the gastrointestinal GI tract require the well-coordinated work of five basic tissue elements: smooth muscle, extrinsic and intrinsic diabetic gastroparesis diet, glial cells, hormonal elements, and the interstitial cells of Cajal ICCs.

Damage to any of these elements leading to an imbalance of the neuromuscular unit will deteriorate the propulsive movement of food to some extent.

The degrees to which these elements are involved determine the degree and nature of the functional kezelése zöldségek cukorbetegség. The stomach, positioned in diabetic gastroparesis diet upper tract of the GI system, has a unique role in the processing of food, since it accommodates to the volume of the aliments, stores them, grinds them into small pieces, and transmits the food toward the duodenum.

Under physiological conditions, the movement of low-calory liquid food, especially water, toward the duodenum depends on its volume and the pressure pump function of the stomach [1]. Low-calory solid food such as bread spends 20—30 min in the stomach, while a continuous peristaltic movement starts at the mid-upper corpus of the greater curvature of the stomach, spreads toward the antral region usually 3—5 times per minute [2], and presses the pieces of food to the almost closed pylorus.

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This way, the stomach comminutes the solid food and makes it accessible to the digestive enzymes. Hyperosmotic, acidic, or nutrient-rich food makes stomach emptying much slower [3]. The over-slow emptying of solid food from the stomach for a nonmechanical reason is defined as gastroparesis [4].

Gastroparesis was one of the first complications of diabetes described diabetic gastroparesis diet, and some ancient doctors, such as Aretaeus of Cappadocia, thought that diabetes was a disease of the stomach. The etiology of gastroparesis cannot be identified in about a third of the cases [6]. The symptoms in all cases are chronic and recur frequently [7], including epigastric burning sensation, bloating, early satiety, abdominal discomfort, nausea, and vomiting.

Diabetic gastroparesis occurs more frequently in women, in obese patients with poor glycemic control, and in patients where other complications of diabetes have already appeared. Nonetheless, an obvious relationship between the higher glycated hemoglobin HbA1c level and the development and severity of gastroparesis has not been clearly established [9]. The connection between symptoms and motility disorders related to gastroparesis is rather poor [17, 18].

diabetic gastroparesis diet

An increased rate of stomach emptying is a characteristic finding in patients with a relatively short diabetes history less than 2 years and without the signs and symptoms of diabetic neuropathy [19]. Faster than normal stomach emptying can be observed even in long-term type 1 diabetes diabetic gastroparesis diet [12]. In animal models, insulin therapy in a subtherapeutic dosage normalized increased stomach emptying [20].

The most important consequence of faster gastric emptying in clinical practice is sudden postprandial hyperglycemia shortly following food intake. It is also possible that this increased rate of stomach emptying is a preliminary phase of later slower stomach emptying [21].

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Diabetic gastroparesis involves a severe delay of stomach emptying of both solid and liquid food [22]. In a survey, type 2 diabetic patients with delayed emptying were older, had higher body mass index, and exhibited more intensive nausea and early satiety, as compared with type 1 diabetic patients Curr Diab Rep with impaired gastric motility [23].

Several functional changes can be found in the diabetic gastroparesis diet of slower stomach diabetic gastroparesis diet [21—24]. However, acute and chronic hyperglycemia have diabetic gastroparesis diet effects on stomach motility. In healthy volunteers, severe artificial hyperglycemia causes slowing-down of the emptying of nutrient-containing liquid and solid food [25]. In type 1 diabetic patients with diabetic autonomic neuropathy, hyperglycemia increases the frequency of rhythmic activity in the stomach, resulting in tachygastria [26].

Obvious deleterious effects of hyperglycemia cannot be cukorbetegség vizeletinkontinencia kezelésére on ICCs cells generate and propagate electrical activity in the stomach and the GI tract diabetic gastroparesis diet.

Interestingly, in type 1 diabetic patients without autonomic neuropathy, the stomach emptying can be significantly decreased even if the postprandial blood glucose elevation does not exceed the physiological range [28]. Chronic hyperglycemia in diabetes can also be responsible for all of the above-mentioned motility disorders.

However, it is important to consider that diabetes is associated not only with elevated blood glucose levels, but additionally with an absolute or relative absence of insulin. The importance of this phenomenon is revealed by in vitro experimental data demonstrating the deteriorating effect of the absolute absence of insulin on stomach ICCs and the smooth muscle cells [27]. In general, slower movement of solid food from the stomach in diabetes is more frequent than slower movement of liquids.

The impaired pyloric pressure pump function also has an effect on solid food emptying [29], and the dilatation of the distal stomach also relates to the antral hypomotility [30]. It is probably important that the slow waves of the stomach generated by the ICCs are modified by a number of factors, such as the sympathetic—parasympathetic balance, eating, and medicines. Any disturbance in these factors can worsen the effectivity of the peristalsis [18].

Evaluation of Diagnostic Methods and Dietary Treatment of Diabetic Gastroparesis

The reasons for the discrepancy between the symptoms and detectable motility disorders are not clear; a possible explanation is the viscero-sensory functional defect related to diabetic autonomic neuropathy. The increased activity or sensitivity of these neuronal systems in the proximal stomach might explain the generation of nausea, vomiting, early satiety, and epigastrial pain experienced in type 1 diabetic patients diabetic gastroparesis diet substantial motility disorders [32].

Various factors can damage different tissues, including hyperglycemia and an absolute or Page 3 of 9, relative lack of insulin.

diabetic gastroparesis diet

The increase in mitochondrial superoxide activity caused by the increased glucose burden can be an important factor in the development of chronic morphologic complications of diabetes [33].

The increased oxidative stress-related decrease in nitric oxide NO concentration, together with the reduced activity of heme oxygenase, is an important feature of the pathogenetic background at the cellular level [34]. Carbon monoxide produced by heme oxygenase has a protective effect on the ICCs [35]. Histological changes in long-standing diabetes can also be studied.

In a human investigation in antrum samples, mild lymphocytic infiltration in the myenteric plexus was a characteristic finding of diabetic gastroparesis [36].

diabetic gastroparesis diet

Significant reductions in the numbers of neuronal elements and the ICCs in the antrum wall were detected [37]. In another investigation, the loss of neuronal elements was proven in diabetic samples from the mucosal layer [38].

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In a larger study [39], the most frequent abnormality was damage to or loss of the ICCs and the decrease in the diabetic gastroparesis diet of NO synthase NOS positive neurons. However, the loss of the NOS-positive neurons was more characteristic for idiopathic gastroparesis. Electromicroscopic investigations detected a significant increase in the amount of connective tissue.

Overall, the most characteristic histopathological change in diabetic gastroparesis is the loss of or damage to the ICCs. The pathophysiologic steps leading to ICC damage are complex.

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