Abnormal Ghrelin and Pancreatic Polypeptide Responses in Gastroparesis

Gaddipati, Kishore; Simonian, Hrair P.; Kresge, Karen; Boden, Guenther; Parkman, Henry P.

doi:10.1007/s10620-005-9022-z

Cited by 49 publications

(42 citation statements)

References 35 publications

(37 reference statements)

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“…These findings are in accordance with a study of Gaddipati et al [14]. Those authors studied the ghrelin and pancreatic polypeptide responses in healthy subjects and patients with diabetic, idiopathic, or postsurgical gastroparesis after sham feeding as a measure of vagal integrity.…”

Section: Discussionsupporting

confidence: 91%

Ghrelin and Obestatin Levels in Type 2 Diabetic Patients With and Without Delayed Gastric Emptying

Harsch

Koebnick²,

Tasi

et al. 2008

Dig Dis Sci

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Alterations in the neurohumoral regulation of the upper intestine may change rhythmicity and pattern of ghrelin and obestatin, the latter presumably antagonizing ghrelin effects. Five nongastroparetic diabetic patients and five with gastroparesis were investigated. Over 390 min including breakfast and lunch, ghrelin was significantly lower in patients with gastroparesis compared with in those without (P = 0.015). Ghrelin subsequent to lunch decreased significantly (P = 0.011) in patients without gastroparesis, but not in gastroparetic patients (P = 0.669). Obestatin was similar in both groups and unchanged. No significant differences in ghrelin-to-obestatin ratio were observed (P = 0.530). Loss of rhythmicity in the ghrelin levels of gastroparetic diabetics highlights the importance of integrity of the neurohumoral-intestinal axis. Stable diurnal obestatin levels do not support the concept of interaction between ghrelin and obestatin in terms of regulation of food intake and gastric emptying.

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Section: Discussionsupporting

confidence: 91%

Ghrelin and Obestatin Levels in Type 2 Diabetic Patients With and Without Delayed Gastric Emptying

Harsch

Koebnick²,

Tasi

et al. 2008

Dig Dis Sci

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“…Ghrelin stimulates short-term food intake, promotes gastric emptying, and regulates body weight. In patients with anorexia or post-bariatric surgery, profound changes in plasma ghrelin levels were found, suggesting that it is an important hormone in the regulation of body weight (Gaddipati et al 2006;Jürimäe et al 2007). Studies on the effects of acute or chronic exercise showed that high-intensity exercise could lower plasma ghrelin levels in rats (Ghanbari-Niaki et al 2008;Wang et al 2008;GhanbariNiaki et al 2009).…”

mentioning

confidence: 99%

Vagal Nerve Regulation Is Essential for the Increase in Gastric Motility in Response to Mild Exercise

Wang

Kondo

Suzukamo

et al. 2010

Tohoku J. Exp. Med.

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It has been shown that mild to moderate exercise can accelerate gastric emptying in humans. However, understanding of the underlying mechanism is hampered by the lack of appropriate animal models. To investigate the effects of mild exercise on gastric motility, we developed an animal model, in which strain gauge transducers were surgically planted on the antral surfaces of female Sprague-Dawley rats. We continuously recorded the contractions of gastric circular muscle in unrestrained conscious rats, divided into four groups: sham-operated exercise, sham-operated sedentary, vagotomized exercise, and vagotomized sedentary. The rats were trained for 3 weeks, and gastric motility was monitored before and after exercise. Although exercise accelerates gastric antral contraction in sham-operated rats, this effect was absent in the vagotomized exercise group, indicating the involvement of the vagal nerve in the exercise-mediated increase in gastric motility. Among the four groups, daily food intake was highest in the sham-operated exercise group. In contrast, the vagotomized exercise group exhibited the smallest body weight gain. Severe gastric retention was observed in vagotomized rats, suggesting a role of the vagal nerve in facilitating food movement and digestion in the stomach. Moreover, at the end of the 3-week exercise, there were no differences in plasma levels of growth hormone, peptid YY, and ghrelin among the four groups. These results indicate that in response to a mild physical exercise challenge, the vagal nerve stimulates gastric motility and enhances the ability of the stomach to process food. Our findings highlight the significance of neuronal control of stomach function.

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“…Thus, suppression of ghrelin by food or an oral glucose load may not be regulated by the plasma level of glucose and/or insulin, but rather by some direct or indirect information from the gastrointestinal tract. Very recently, Gaddipati et al reported that sham feeding could increase the plasma ghrelin level in normal subjects, while such a response of ghrelin was not observed in patients with diabetic gastroparesis [27]. In contrast, Arosio et al reported that circulating ghrelin concentrations decreased with sham feeding as they do with actual meal ingestion in humans [28].…”

Section: Discussionmentioning

confidence: 99%

No Ghrelin Response to Oral Glucose in Diabetes Mellitus with Gastroparesis

et al. 2009

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Abstract. To investigate the role of ghrelin, an endogenous ligand of the growth hormone secretagogue receptor, in diabetic gastroparesis, we evaluated the plasma ghrelin profile during the oral glucose tolerance test in 55 patients with diabetes (men/women: 36/19, mean ± SE of age: 55.1 ± 1.7 years) with or without gastroparesis (diagnosed by the 13 Cacetate breath test). We also further examined cardiac autonomic neuropathy by assessing 24-hour variation of the R-R interval in randomly selected 32 patients with diabetes (men/women: 23/9, mean ± SE of age: 54.2 ± 2.5 years), and evaluated the influence of autonomic neuropathy on ghrelin. The fasting plasma ghrelin level was significantly lower in diabetes mellitus with gastroparesis than in healthy controls (7.9 ± 0.7 fmol/ml versus 16.6 ± 5.3 fmol/ml, p = 0.006). Patients with diabetes with gastroparesis showed no decrease of plasma ghrelin after glucose loading, unlike patients without gastroparesis or healthy controls. Diabetes mellitus with autonomic neuropathy, but not those without it, also showed no decrease of plasma ghrelin after glucose loading. Diabetic gastroparesis may be related to ghrelin-associated neurohormonal abnormalities, but the pathophysiological meaning of this abnormal ghrelin response needs further clarification.

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Abnormal Ghrelin and Pancreatic Polypeptide Responses in Gastroparesis

Cited by 49 publications

References 35 publications

Ghrelin and Obestatin Levels in Type 2 Diabetic Patients With and Without Delayed Gastric Emptying

Ghrelin and Obestatin Levels in Type 2 Diabetic Patients With and Without Delayed Gastric Emptying

Vagal Nerve Regulation Is Essential for the Increase in Gastric Motility in Response to Mild Exercise

No Ghrelin Response to Oral Glucose in Diabetes Mellitus with Gastroparesis

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