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Gallbladder and Gastric Motility in Obese Children and Adults

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Gallbladder and Gastric Motility in Obese Children and Adults

Abstract and Introduction

Abstract


Background and Aim: Impaired gallbladder and gastric motility have been associated with obesity in adults. The timing of appearance of this dysfunction, however, is unclear.
Methods: Lean and obese subjects from three different age groups were studied noninvasively: 50 newborns (1–12 months old, six obese), 18 pre-adolescents (7–8 years old, seven obese), and 99 adults (22–80 years old, 32 obese) classified according to standard normal tables and body mass index. Changes of fasting/postprandial gallbladder and gastric motility were assessed simultaneously by functional ultrasonography in response to milk (newborns and pre-adolescents) and to a liquid test meal (adults).
Results: In newborns, fasting and postprandial gallbladder volumes and gastric emptying were similar between obese and lean subjects. In pre-adolescents, obese subjects had a larger fasting gallbladder volume, with slower postprandial gastric emptying than lean subjects. In obese adults, the most evident dysfunction emerged, with larger fasting and postprandial residual gallbladder volume, and slower postprandial gastric emptying than lean subjects.
Conclusions: Obese subjects display abnormal gallbladder and gastric motility patterns, which first appear in pre-adolescents and deteriorate in adults. Such abnormalities are absent in obese newborns. Functional ultrasonography can detect altered cholecysto-gastric motility at the earliest stage. Our findings suggest an age-related decline of motility, probably secondary to excessive fat and insulin-resistance.

Introduction


Obesity is spreading worldwide and is a major public health problem in westernized countries. The presence of obesity alone or as a component of the metabolic syndrome, is a predisposing factor for gallstone disease in adults. Of note, the increasing prevalence of obesity is heavily affecting children and adolescents as well, and as the prevalence of obesity increases, so does the prevalence of potentially harmful comorbidities associated with obesity, including cholesterol gallstones and liver steatosis. Coordinate neurohormonal regulation of gallbladder motor function and mucosal absorptive-secretory function in the interprandial and postprandial phases are essential features to promote bile storage, concentration, and delivery to the intestine, as well as to prevent early crystallization and precipitation of excess biliary cholesterol, which accumulates as gallstone growth. Impaired gallbladder motility, irrespective of stone size and gallbladder inflammation, can antedate gallstone formation in both humans and animal models of cholesterol gallstones. Previous studies pointed to the presence of an altered gallbladder and gastric motility in adult obese subjects. Time of appearance of motility dysfunctions, however, is not fully understood. Although the prevalence of gallstone disease is low in children and adolescents, the risk of developing gallstones increases as the body mass index (BMI) and obesity increase in youth and continues. In a large epidemiological study conducted in southern Italy, we have previously shown that fasting gallbladder volume was increased in obese children compared to lean subjects. This finding points to a form of gallbladder stasis, a clear predisposing factor to gallstone disease. Prior studies in adults suggested that impaired gallbladder motor functions may also be associated with abnormal gastric emptying in childhood; until now, however, this information is lacking in obese children.

We aimed therefore to examine the impact of obesity on gallbladder and gastric motility in different age groups, from newborns to adults, as well as to study whether alterations of the motility pattern during childhood are similar to those previously described in adults.

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