Glucagon-Like Peptide 2 Enhances Maltase-Glucoamylase and Sucrase-Isomaltase Gene Expression and Activity in Parenterally Fed Premature Neonatal Piglets

PETERSEN, Y. M.

doi:10.1203/01.pdr.0000030884.86822.e4

Cited by 11 publications

(13 citation statements)

References 23 publications

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“…The increase in brush border enzyme activities, particularly sucrase and maltase in GLP-2-treated pigs, is in agreement with previous findings in rodents (40) and unresected preterm and term pigs (30,31). On the other hand, GLP-2 had no effect on tissue-specific nutrient (glucose, leucine) transport and in vivo galactose uptake, which is consistent with our previous findings, showing hyporesponsiveness in fetal and preterm compared with term piglets (34,37,38).…”

Section: Discussionsupporting

confidence: 93%

“…In adult patients with SBS, exogenous GLP-2 improves intestinal adaptation and stimulates intestinal function (20), but evidence is lacking regarding the effects of GLP-2 in SBS newborns. GLP-2 stimulates growth and function of the intact intestine of TPN-fed preterm and term pigs (30,31), but the efficacy appears diminished in preterm pigs (34). In this study, we combined an immature state of the intestine with SBS and jejunostomy in preterm pigs.…”

Section: Discussionmentioning

confidence: 99%

“…The rapid intestinal growth and maturation in neonates appears to be GLP-2 mediated (32), and exogenous GLP-2 is known to stimulate intestinal brush-border enzyme expression and decrease apoptosis and proteolysis in preterm pigs (4,31). Furthermore, GLP-2 increases nutrient absorption (37) and stimulates intestinal blood flow in piglets (13,14).…”

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confidence: 99%

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Glucagon-like peptide-2 induces rapid digestive adaptation following intestinal resection in preterm neonates

Vegge

Thymann

Lund

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

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Short bowel syndrome (SBS) is a frequent complication after intestinal resection in infants suffering from intestinal disease. We tested whether treatment with the intestinotrophic hormone glucagon-like peptide-2 (GLP-2) increases intestinal volume and function in the period immediately following intestinal resection in preterm pigs. Preterm pigs were fed enterally for 48 h before undergoing resection of 50% of the small intestine and establishment of a jejunostomy. Following resection, pigs were maintained on total parenteral nutrition (TPN) without (SBS, n = 8) or with GLP-2 treatment (3.5 μg/kg body wt per h, SBS+GLP-2, n = 7) and compared with a group of unresected preterm pigs (control, n = 5). After 5 days of TPN, all piglets were fed enterally for 24 h, and a nutrient balance study was performed. Intestinal resection was associated with markedly reduced endogenous GLP-2 levels. GLP-2 increased the relative absorption of wet weight (46 vs. 22%), energy (79 vs. 64%), and all macronutrients (all parameters P < 0.05). These findings were supported by a 200% increase in sucrase and maltase activities, a 50% increase in small intestinal epithelial volume (P < 0.05), as well as increased DNA and protein contents and increased total protein synthesis rate in SBS+GLP-2 vs. SBS pigs (+100%, P < 0.05). Following intestinal resection in preterm pigs, GLP-2 induced structural and functional adaptation, resulting in a higher relative absorption of fluid and macronutrients. GLP-2 treatment may be a promising therapy to enhance intestinal adaptation and improve digestive function in preterm infants with jejunostomy following intestinal resection.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

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Glucagon-like peptide-2 induces rapid digestive adaptation following intestinal resection in preterm neonates

Vegge

Thymann

Lund

et al. 2013

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…GLP-2 treatment during TPN maintained lactasespecific activity and hence digestive capacity, consistent with other findings for lactase and other BBM disaccharides in piglets and mice (2,(33)(34)(35). Moreover, the GLP-2 treatment maintained lactose digestive capacity at a level twice that of TPN-fed piglets and approximately four times higher that the lactose intake during refeeding.…”

Section: Discussionsupporting

confidence: 89%

Glucagon-like peptide-2 protects against TPN-induced intestinal hexose malabsorption in enterally refed piglets

Cottrell

Stoll

Buddington

et al. 2006

American Journal of Physiology-Gastrointestinal and Liver Physi

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Premature infants receiving chronic total parenteral nutrition (TPN) due to feeding intolerance develop intestinal atrophy and reduced nutrient absorption. Although providing the intestinal trophic hormone glucagon-like peptide-2 (GLP-2) during chronic TPN improves intestinal growth and morphology, it is uncertain whether GLP-2 enhances absorptive function. We placed catheters in the carotid artery, jugular and portal veins, duodenum, and a portal vein flow probe in piglets before providing either enteral formula (ENT), TPN or a coinfusion of TPN plus GLP-2 for 6 days. On postoperative day 7, all piglets were fed enterally and digestive functions were evaluated in vivo using dual infusion of enteral ((13)C) and intravenous ((2)H) glucose, in vitro by measuring mucosal lactase activity and rates of apical glucose transport, and by assessing the abundances of sodium glucose transporter-1 (SGLT-1) and glucose transporter-2 (GLUT2). Both ENT and GLP-2 pigs had larger intestine weights, longer villi, and higher lactose digestive capacity and in vivo net glucose and galactose absorption compared with TPN alone. These endpoints were similar in ENT and GLP-2 pigs except for a lower intestinal weight and net glucose absorption in GLP-2 compared with ENT pigs. The enhanced hexose absorption in GLP-2 compared with TPN pigs corresponded with higher lactose digestive and apical glucose transport capacities, increased abundance of SGLT-1, but not GLUT-2, and lower intestinal metabolism of [(13)C]glucose to [(13)C]lactate. Our findings indicate that GLP-2 treatment during chronic TPN maintains intestinal structure and lactose digestive and hexose absorptive capacities, reduces intestinal hexose metabolism, and may facilitate the transition to enteral feeding in TPN-fed infants.

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“…On the basis of the integrity of the 18S and 28S bands, only samples showing no sign of degradation were chosen for further evaluation. RNA was reverse transcribed into cDNA as described previously (30).…”

Section: Rna Extraction and Reverse Transcriptionmentioning

confidence: 99%

Preterm birth makes the immature intestine sensitive to feeding-induced intestinal atrophy

Bjørnvad

Schmidt²,

Petersen³

et al. 2005

American Journal of Physiology-Regulatory, Integrative and Comp

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Preterm birth and formula feeding predispose to small intestinal dysfunction, which may lead to necrotizing enterocolitis (NEC). In piglets, we tested whether the physiological and environmental transitions occurring at birth affect the response of the immature intestine to enteral feeding. Pig fetuses (106 days gestation, term = 115 days) were prepared with esophageal feeding tubes and fed either sow's colostrum (n = 8) or infant formula (n = 7) in utero. After 24 h of oral feeding, the pig fetuses were delivered by cesarean section and their gastrointestinal morphology and function were compared with those of preterm newborn (NB) littermates that were not fed (n = 8) or fed colostrum (n = 7) or formula (n = 13) for 24 h after birth. Before birth, both colostrum and formula feeding resulted in marked increases in intestinal mass, brush-border enzyme activities, and plasma glucagon-like peptide 2 concentrations, to levels similar to those in NB colostrum-fed piglets. In contrast, NB formula-fed piglets showed reduced intestinal growth, decreased brush-border enzyme activities, and intestinal lesions, reflecting NEC. NB formula-fed pigs also showed impaired enterocyte endocytotic function and decreased antioxidative capacity, whereas brush-border enzyme mRNA levels were unaltered, relative to NB colostrum-fed pigs. Our results indicate that the feeding-induced growth and enzyme maturation of the immature intestine are not birth dependent. However, with a suboptimal diet (milk formula), factors related to preterm birth (e.g., microbial colonization and metabolic and endocrine changes) make the immature intestine sensitive to atrophy and development of NEC.

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Glucagon-Like Peptide 2 Enhances Maltase-Glucoamylase and Sucrase-Isomaltase Gene Expression and Activity in Parenterally Fed Premature Neonatal Piglets

Cited by 11 publications

References 23 publications

Glucagon-like peptide-2 induces rapid digestive adaptation following intestinal resection in preterm neonates

Glucagon-like peptide-2 induces rapid digestive adaptation following intestinal resection in preterm neonates

Glucagon-like peptide-2 protects against TPN-induced intestinal hexose malabsorption in enterally refed piglets

Preterm birth makes the immature intestine sensitive to feeding-induced intestinal atrophy

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