Refeeding improves blood glucose and gastric emptying responses to a mixed-nutrient meal in anorexia nervosa

Postprandial glucose is reduced in malnourished patients with anorexia nervosa (AN), but the mechanisms and duration for this remain unclear. We examined blood glucose, gastric emptying, and glucoregulatory hormone changes in malnourished patients with AN and during 2 wk of acute refeeding compared with healthy controls (HCs). Twenty-two female adolescents with AN and 17 age-matched female HCs were assessed after a 4-h fast. Patients were commenced on a refeeding protocol of 2,400 kcal/day. Gastric emptying (13C-octanoate breath test), glucose absorption (3-O-methylglucose), blood glucose, plasma glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), insulin, C-peptide, and glucagon responses to a mixed-nutrient test meal were measured on admission and 1 and 2 wk after refeeding. HCs were assessed once. On admission, patients had slower gastric emptying, lower postprandial glucose and insulin, and higher glucagon and GLP-1 than HCs ( P < 0.05). In patients with AN, the rise in glucose (0–30 min) correlated with gastric emptying ( P < 0.05). With refeeding, postprandial glucose and 3-O-methylglucose were higher, gastric emptying faster, and baseline insulin and C-peptide less ( P < 0.05), compared with admission. After 2 wk of refeeding, postprandial glucose remained lower, and glucagon and GLP-1 higher, in patients with AN than HCs ( P < 0.05) without differences in gastric emptying, baseline glucagon, or postprandial insulin. Delayed gastric emptying may underlie reduced postprandial glucose in starved patients with AN; however, postprandial glucose and glucoregulatory hormone changes persist after 2 wk of refeeding despite improved gastric emptying. Future research should explore whether reduced postprandial glucose in AN is related to medical risk by examining associated symptoms alongside continuous glucose monitoring during refeeding.

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Effect of commercial rye whole-meal bread on postprandial blood glucose and gastric emptying in healthy subjects

Nutrition Journal ◽

10.1186/1475-2891-8-26 ◽

2009 ◽

Vol 8 (1) ◽

Cited By ~ 12

Author(s):

Joanna Hlebowicz ◽

Jenny Maria Jönsson ◽

Sandra Lindstedt ◽

Ola Björgell ◽

Gassan Darwich ◽

...

Keyword(s):

Blood Glucose ◽

Gastric Emptying ◽

Healthy Subjects ◽

Postprandial Blood Glucose

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The effect of incorporating fat into different components of a meal on gastric emptying and postprandial blood glucose and insulin responses

British Journal Of Nutrition ◽

10.1079/bjn19890116 ◽

1989 ◽

Vol 61 (2) ◽

pp. 285-290 ◽

Cited By ~ 60

Author(s):

K. M. Cunningham ◽

N. W. Read

Keyword(s):

Blood Glucose ◽

Gastric Emptying ◽

Delayed Gastric Emptying ◽

The Other ◽

Postprandial Blood Glucose ◽

Lag Phase ◽

Normal Volunteers ◽

Insulin Responses

1. Three studies were carried out in each of six normal volunteers to investigate how lipid, when given at different stages during the course of a meal, affects gastric emptying and postprandial blood glucose and insulin concentrations.2. The control meal consisted of 300 ml beef consommé (50 kJ, 12 kcal), followed 20 min later by 300 g mashed potato (908 kJ, 217 kcal). In the two test meals, 60 g margarine were incorporated into either the soup or the mashed potato.3. The addition of margarine to either component of the meal delayed gastric emptying of the mashed potato (P< 0.05), but the pattern varied according to the component to which the fat was added.4. Incorporation of fat into the soup increased the lag phase (P< 0.05) but did not influence the slope of emptying of the mashed potato, while incorporation of fat into the mashed potato reduced the slope of emptying of the mashed potato (P< 0.05) but did not influence the lag phase.5. Addition of fat to either component of the meal reduced postprandial blood glucose (P< 0.05) and insulin responses, but when the fat was incorporated in the soup, peak glucose and insulin responses were delayed as well (P< 0.05).6. The results show that the effect of fat on gastric emptying and absorption of nutrients depends on when, in relation to the other components of the meal, the fat is consumed.

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Primary anorexia nervosa: Gastric emptying and antral motor activity in 53 patients

International Journal of Eating Disorders ◽

10.1002/1098-108x(199203)11:2<163::aid-eat2260110207>3.0.co;2-r ◽

1992 ◽

Vol 11 (2) ◽

pp. 163-172 ◽

Cited By ~ 21

Author(s):

Georg Stacher ◽

Helmar Bergmann ◽

Stefan Wiesnagrotzki ◽

Gerda Steiner-Mittelbach ◽

Alexander Kiss ◽

...

Keyword(s):

Anorexia Nervosa ◽

Gastric Emptying ◽

Motor Activity

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LPS inhibits fasted plasma ghrelin levels in rats: role of IL-1 and PGs and functional implications

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00533.2005 ◽

2006 ◽

Vol 291 (4) ◽

pp. G611-G620 ◽

Cited By ~ 56

Author(s):

Lixin Wang ◽

Nicole R. Basa ◽

Almaas Shaikh ◽

Andrew Luckey ◽

David Heber ◽

...

Keyword(s):

Blood Glucose ◽

Gastric Emptying ◽

Food Intake ◽

Intravenous Injection ◽

Plasma Levels ◽

Inhibitory Action ◽

Functional Implications ◽

Urocortin 1 ◽

Fasted Rats

LPS injected intraperitoneally decreases fasted plasma levels of ghrelin at 3 h postinjection in rats. We characterized the inhibitory action of LPS on plasma ghrelin and whether exogenous ghrelin restores LPS-induced suppression of food intake and gastric emptying in fasted rats. Plasma ghrelin and insulin and blood glucose were measured after intraperitoneal injection of LPS, intravenous injection of IL-1β and urocortin 1, and in response to LPS under conditions of blockade of IL-1 or CRF receptors by subcutaneous injection of IL-1 receptor antagonist (IL-1Ra) or astressin B, respectively, and prostaglandin (PG) synthesis by intraperitoneal indomethacin. Food intake and gastric emptying were measured after intravenous injection of ghrelin at 5 h postintraperitoneal LPS injection. LPS inhibited the elevated fasted plasma ghrelin levels by 47.6 ± 4.9%, 58.9 ± 3.3%, 74.4 ± 2.7%, and 48.9 ± 8.7% at 2, 3, 5, and 7 h postinjection, respectively, and values returned to preinjection levels at 24 h. Insulin levels were negatively correlated to those of ghrelin, whereas there was no significant correlation between glucose and ghrelin. IL-1Ra and indomethacin prevented the first 3-h decline in ghrelin levels induced by LPS, whereas astressin B did not. IL-1β inhibited plasma ghrelin levels, whereas urocortin 1 had no influence. Ghrelin injected intravenously prevented an LPS-induced 87% reduction of gastric emptying and 61% reduction of food intake. These data showed that IL-1 and PG pathways are part of the early mechanisms by which LPS suppresses fasted plasma ghrelin and that exogenous ghrelin can normalize LPS-induced-altered digestive functions.

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Effect of insulin-induced hypoglycaemia on antral, pyloric and duodenal motility in fasting subjects

Clinical Science ◽

10.1042/cs0810281 ◽

1991 ◽

Vol 81 (2) ◽

pp. 281-285 ◽

Cited By ~ 4

Author(s):

R. Fraser ◽

J. Fuller ◽

M. Horowitz ◽

J. Dent

Keyword(s):

Blood Glucose ◽

Gastric Emptying ◽

Phase I ◽

Blood Glucose Concentration ◽

Migrating Motor Complex ◽

Control Group ◽

Motor Complex ◽

Significant Difference ◽

Interdigestive Migrating Motor Complex ◽

Pyloric Motility

1. Hyperglycaemia alters gastric motility and delays gastric emptying. By contrast, there is little information regarding the effect of sub-normal blood glucose concentrations on gastric and, in particular, pyloric motility, although limited data suggest that hypoglycaemia is associated with accelerated gastric emptying despite an apparently increased basal pyloric pressure. 2. To determine the effects of hypoglycaemia on pyloric motility, we compared the effects of an intravenous injection of insulin (0.15 units/kg) with those of a placebo injection of saline in eight healthy human volunteers during phase I of the interdigestive migrating motor complex. 3. All subjects developed profound hypoglycaemia (mean blood glucose concentration 1.6 mmol/l compared with 4.0 mmol/l in the control group). 4. There was no significant difference in the number of antral (9 versus 7, P = 0.34), pyloric (3 versus 0, P = 0.31) or duodenal (21 versus 13, P = 0.42) pressure waves or in the basal pyloric pressure (0.3 mmHg versus 0.1 mmHg, P = 0.37) in the 45 min after insulin injection (hypoglycaemia) when compared with the 45 min after saline injection (euglycaemia). In both the euglycaemic and hypoglycaemic studies there was a time-dependent increase in the numbers of antral and duodenal waves consistent with the expected changes in the interdigestive migrating motor complex. 5. These results indicate that insulin-induced hypoglycaemia has no significant effect on pyloric motility during phase I of the interdigestive migrating motor complex.

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Effect of the artificial sweetener, sucralose, on gastric emptying and incretin hormone release in healthy subjects

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.90708.2008 ◽

2009 ◽

Vol 296 (4) ◽

pp. G735-G739 ◽

Cited By ~ 155

Author(s):

Jing Ma ◽

Max Bellon ◽

Judith M. Wishart ◽

Richard Young ◽

L. Ashley Blackshaw ◽

...

Keyword(s):

Blood Glucose ◽

Gastric Emptying ◽

Normal Saline ◽

Sweet Taste ◽

Artificial Sweetener ◽

Healthy Humans ◽

Sweet Taste Receptors ◽

Glucagon Like Peptide 1 ◽

Gip Release ◽

Glucose Plasma

The incretin hormones, glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide (GIP), play an important role in glucose homeostasis in both health and diabetes. In mice, sucralose, an artificial sweetener, stimulates GLP-1 release via sweet taste receptors on enteroendocrine cells. We studied blood glucose, plasma levels of insulin, GLP-1, and GIP, and gastric emptying (by a breath test) in 7 healthy humans after intragastric infusions of 1) 50 g sucrose in water to a total volume of 500 ml (∼290 mosmol/l), 2) 80 mg sucralose in 500 ml normal saline (∼300 mosmol/l, 0.4 mM sucralose), 3) 800 mg sucralose in 500 ml normal saline (∼300 mosmol/l, 4 mM sucralose), and 4) 500 ml normal saline (∼300 mosmol/l), all labeled with 150 mg 13C-acetate. Blood glucose increased only in response to sucrose ( P < 0.05). GLP-1, GIP, and insulin also increased after sucrose ( P = 0.0001) but not after either load of sucralose or saline. Gastric emptying of sucrose was slower than that of saline ( t50: 87.4 ± 4.1 min vs. 74.7 ± 3.2 min, P < 0.005), whereas there were no differences in t50 between sucralose 0.4 mM (73.7 ± 3.1 min) or 4 mM (76.7 ± 3.1 min) and saline. We conclude that sucralose, delivered by intragastric infusion, does not stimulate insulin, GLP-1, or GIP release or slow gastric emptying in healthy humans.

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