Reduced postprandial blood glucose levels in recently diagnosed non-insulin-dependent diabetics secondary to pharmacologically induced delayed gastric emptying

Phillips, William T.; Schwartz, Joyce G.; McMahan, C. Alex

doi:10.1007/bf01296773

Cited by 47 publications

(32 citation statements)

References 30 publications

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“…It has been reported in humans both in early NIDDM [1,4], and in insulin-dependent diabetic (IDDM) patients who were asymptomatic for gastrointestinal dysfunction [12]. In rats, accelerated gastric emptying of liquid or solid meals was previously demonstrated in several models of IDDM [13,14].…”

Section: Discussionmentioning

confidence: 99%

“…Intravenous CCK at physiological doses normalized the accelerated gastric emptying rates in patients with NIDDM [4] and improved indices of glucose control, i. e. postprandial blood glucose and insulin values were lowered. Therefore, it seemed worthwhile to establish an appropriate animal model to test compounds known to release endogenous CCK for their ability to slow gastric emptying and improve postprandial hyperglycaemia in NIDDM.…”

Section: Discussionmentioning

confidence: 99%

“…Intravenous administration of cholecystokinin (CCK), a physiological inhibitor of gastric emptying in healthy humans [3], normalized gastric emptying of a glucose test meal in NIDDM diabetic patients and reduced the postprandial hyperglycaemia [4]. This outcome was predicted from studies in healthy human subjects which showed that CCK regulated postprandial blood glucose levels by slowing gastric emptying [5].…”

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confidence: 98%

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Accelerated gastric emptying of glucose in Zucker type 2 diabetic rats: role in postprandial hyperglycaemia

et al. 1997

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Phillips et al. [1] demonstrated abnormally rapid gastric emptying of glucose solutions in patients with recently diagnosed non-insulin-dependent diabetes mellitus (NIDDM), which contrasts with delayed gastric emptying (gastroparesis), a well-documented late manifestation of diabetes attributed to autonomic neuropathy [2]. Intravenous administration of cholecystokinin (CCK), a physiological inhibitor of gastric emptying in healthy humans [3], normalized gastric emptying of a glucose test meal in NIDDM diabetic patients and reduced the postprandial hyperglycaemia [4]. This outcome was predicted from studies in healthy human subjects which showed that CCK regulated postprandial blood glucose levels by slowing gastric emptying [5]. These studies support the hypothesis [1] that accelerated gastric emptying in early NIDDM in humans may contribute to poor glucose control by increasing the rate of glucose entry into the small intestine, thereby increasing absorption rate and exacerbating postprandial hyperglycaemia.To further examine this phenomenon, the gastric emptying of glucose was investigated in a newly Diabetologia (1997) Summary Patients with early non-insulin-dependent diabetes mellitus (NIDDM) empty glucose solutions from their stomachs more rapidly than non-diabetic control subjects, and this exacerbates postprandial hyperglycaemia.To determine if accelerated gastric emptying occurred in a rat model of NIDDM and influenced postprandial hyperglycaemia, gastric emptying of glucose was measured, and the effect of slowing the gastric emptying rate on postprandial hyperglycaemia was observed. We tested eight male obese Zucker diabetic rats and eight age-matched lean Zucker controls at 10-13 weeks of age to measure gastric emptying of glucose (by gamma scintigraphy). Rats fasted overnight were gavaged with 30 % glucose at 1 ml/100 g body weight. Separately, six Zucker diabetic rats and six lean controls were tested for sensitivity to the inhibitory effects of cholecystokinin and secretin on gastric emptying. The diabetic rats emptied glucose significantly faster than controls (t 1/2 = 37.3 ± 1.5 vs 58.8 ± 2.3 min in controls), and aging exaggerated this differential. Camostat, a stimulant of cholecystokinin and secretin release, added to the glucose meal significantly slowed gastric emptying (t 1/2 = 123 ± 23 and 166 ± 19 min, diabetic vs lean, respectively), and significantly reduced postprandial hyperglycaemia in diabetic rats. Compared to Zucker lean controls, Zucker diabetic rats were as sensitive (cholecystokinin) or more sensitive (secretin) to gastrointestinal hormones that inhibit gastric emptying. The results demonstrate accelerated gastric emptying in a rat model of NIDDM, consistant with similar observations in humans with early NIDDM. These results also support the proposal that interventions to slow gastric emptying may improve glucose control in this disease. [Diabetologia (1997) 40: 136-142]

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 98%

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Accelerated gastric emptying of glucose in Zucker type 2 diabetic rats: role in postprandial hyperglycaemia

et al. 1997

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“…Indeed, modi®cation of eating rate pharmacologically, 46 by diet 47 or by gastric restrictive surgery may be a feasible treatment of the metabolic syndrome by reducing the rate of glucose absorption and glucose-stimulated insulin release.…”

Section: Discussionmentioning

confidence: 99%

Metabolic correlates of eating behavior in severe obesity

et al. 2001

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BACKGROUND:The bene®t of spreading energy intake over many small meals (`nibbling') rather than few large ones (`gorging') for control of blood glucose, serum lipids and body fat accretion has been known for 60 y, but the mechanisms are poorly understood. Men exhibit more of a gorging eating pattern than women and are also more prone to the metabolic complications of obesity, as are women with a`male', central distribution of adipose tissue. We have shown correlations between central fat distribution, and other components of the metabolic`Syndrome X' and fatty in®ltration of the liver. Here we study relationships between eating rate and fat distribution and test the hypothesis that gorging might be associated with fatty liver. SUBJECTS AND METHODS:In 30 non-alcoholic, non-diabetic, severely obese women (body mass index, BMI 47 AE 1 kgam 2 ; mean AE s.e.m.) with a mean age of 36 AE 1 y and 16 men (BMI: 52 AE 3) age 38 AE 2 y, who were candidates for anti-obesity surgery, we measured eating rate using an eating monitor, and fat distribution by the waist ± hip circumference ratio (WHR). In addition in the 17 women and 11 men who had surgery, serum lipids were analyzed and routine liver biopsies were evaluated for steatosis by a pathologist blinded to the conditions of the study. RESULTS: Men ate signi®cantly faster than women (188 AE 28 vs 123 AE 9 gamin; P`0.01), and had more liver fat (score: 2.7 AE 03 vs 1.5 AE 0.3; P`0.01), with no statistically signi®cant sex differences in s-cholesterol or s-triglycerides. Eating rate correlated with WHR (r 0.46; P`0.01, n 46), liver fat (r 0.55; P`0.01), and s-triglycerides (r 0.42; P`0.05) adjusting for sex. Liver fat correlated with WHR (r 0.50; P`0.05), s-triglycerides (r 0.70; P`0.01) and s-cholesterol (r 0.50; P`0.05), while there were no signi®cant correlations with BMI or body weight. In multivariate analysis eating rate (32%), meal size (8%) and WHR (6%) contributed 46% of the variance in liver fat. CONCLUSION: We showed increased eating rates in severely obese men and women with central fat distribution. Furthermore, increased eating rates were associated with fatty liver and elevated serum lipids. Eating rate in severely obese women and men may be a determinant of the metabolic syndrome.

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“…Although there is a relationship between subsequent energy intake and gastric emptying (37), this may relate particularly to the intragastric distribution of a meal, particularly the content of the distal stomach (41). GE is also a major determinant of postprandial glycemia in health and type 2 diabetes (20,22,26) so that relatively more rapid emptying may potentially predispose to the development of diabetes (31). GE has been reported to be comparable, faster, and slower in the obese (38).…”

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confidence: 99%

Gastric emptying, mouth-to-cecum transit, and glycemic, insulin, incretin, and energy intake responses to a mixed-nutrient liquid in lean, overweight, and obese males

Seimon

Brennan

Russo

et al. 2013

American Journal of Physiology-Endocrinology and Metabolism

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Seimon RV, Brennan IM, Russo A, Little TJ, Jones KL, Standfield S, Wishart JM, Horowitz M, Feinle-Bisset C. Gastric emptying, mouth-to-cecum transit, and glycemic, insulin, incretin, and energy intake responses to a mixed-nutrient liquid in lean, overweight, and obese males. Am J Physiol Endocrinol Metab 304: E294 -E300, 2013. First published December 4, 2012; doi:10.1152/ajpendo.00533.2012.-Observations relating to the impact of obesity on gastric emptying (GE) and the secretion of gut hormones are inconsistent, probably because of a lack of studies in which GE, gastrointestinal hormone release, and energy intake (EI) have been evaluated concurrently with previous patterns of nutrient intake. GE is known to be a major determinant of postprandial glycemia and incretin secretion in health and type 2 diabetes. The aims of this study were to determine the effects of a mixed-nutrient drink on GE, oro-cecal transit, blood glucose, insulin and incretin concentrations and EI, and the relationship between the glycemic response to the drink with GE in lean, overweight, and obese subjects. Twenty lean, 20 overweight, and 20 obese males had measurements of GE, oro-cecal transit, and blood glucose, insulin, GLP-1, and GIP concentrations for 5 h after ingestion of a mixed-nutrient drink (500 ml, 532 kcal); EI at a subsequent buffet lunch was determined. Habitual EI was also quantified. Glycemic and insulinemic responses to the drink were greater in the obese (both P Ͻ 0.05) when compared with both lean and overweight, with no significant differences in GE, intragastric distribution, oro-cecal transit, incretins, or EI (buffet lunch or habitual) between groups. The magnitude of the rise in blood glucose after the drink was greater when GE was relatively more rapid (r ϭ Ϫ0.55, P Ͻ 0.05). In conclusion, in the absence of differences in habitual EI, both GE and incretin hormones are unaffected in the obese despite greater glucose and insulin responses, and GE is a determinant of postprandial glycemia.glucagon-like peptide-1; glucose-dependent insulinotropic peptide; habitual food intake; blood glucose control GASTROINTESTINAL (GI) function, including pyloric activity, gastric emptying (GE), and intragastric meal distribution, is pivotal to the regulation of appetite (36) and blood glucose homeostasis (20) and accordingly is of relevance to an understanding of the pathogenesis, and for rational management, of obesity. Moreover, macronutrient intake per se modulates GI function and thus potentially appetite regulation in both animals and humans. For example, in rats, exposure to a high-fat diet attenuates the suppressive effects of small intestinal fat on GE (11) and energy intake (12), and there is evidence that the sensitivity to the effects of fat on GI function and energy intake is reduced by a high-fat diet (4,14). Although specific aspects of GI function in the obese have been investigated in a number of studies, there is a lack of studies that have evaluated changes in GI function in lean, overweight, and obese individuals,...

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Reduced postprandial blood glucose levels in recently diagnosed non-insulin-dependent diabetics secondary to pharmacologically induced delayed gastric emptying

Cited by 47 publications

References 30 publications

Accelerated gastric emptying of glucose in Zucker type 2 diabetic rats: role in postprandial hyperglycaemia

Accelerated gastric emptying of glucose in Zucker type 2 diabetic rats: role in postprandial hyperglycaemia

Metabolic correlates of eating behavior in severe obesity

Gastric emptying, mouth-to-cecum transit, and glycemic, insulin, incretin, and energy intake responses to a mixed-nutrient liquid in lean, overweight, and obese males

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