scholarly journals Pancreatic Lipase-related Protein-2 (PLRP2) Can Contribute to Dietary Fat Digestion in Human Newborns

2011 ◽  
Vol 286 (30) ◽  
pp. 26353-26363 ◽  
Author(s):  
Xunjun Xiao ◽  
Amitava Mukherjee ◽  
Leah E. Ross ◽  
Mark E. Lowe
2007 ◽  
Vol 62 (5) ◽  
pp. 537-541 ◽  
Author(s):  
Xiaonan Li ◽  
Susanne Lindquist ◽  
Mark Lowe ◽  
Laila Noppa ◽  
Olle Hernell

1998 ◽  
Vol 273 (47) ◽  
pp. 31215-31221 ◽  
Author(s):  
Mark E. Lowe ◽  
Mark H. Kaplan ◽  
Laurie Jackson-Grusby ◽  
Dymphna D’Agostino ◽  
Michael J. Grusby

2021 ◽  
Vol 12 ◽  
Author(s):  
Guoying Zhu ◽  
Qing Fang ◽  
Fengshang Zhu ◽  
Dongping Huang ◽  
Changqing Yang

Pancreatic lipase is critical for the digestion and absorption of dietary fats. The most abundant lipolytic enzymes secreted by the pancreas are pancreatic triglyceride lipase (PTL or PNLIP) and its family members, pancreatic lipase-related protein 1 (PNLIPRP1or PLRP1) and pancreatic lipase-related protein 2 (PNLIPRP2 or PLRP2). Unlike the family’s other members, PNLIPRP2 plays an elemental role in lipid digestion, especially for newborns. Therefore, if genetic factors cause gene mutation, or other factors lead to non-expression, it may have an effect on fat digestion and absorption, on the susceptibility to pancreas and intestinal pathogens. In this review, we will summarize what is known about the structure and function of PNLIPRP2 and the levels of PNLIPRP2 and associated various pathological states.


2005 ◽  
Vol 94 (6) ◽  
pp. 885-889 ◽  
Author(s):  
Ruth Z. Birk ◽  
Karen S. Regan ◽  
Patsy M. Brannon

Lactation alters maternal metabolism and increases food intake in rats to support milk production. Pancreatic lipase (PL) is primarily responsible for fat digestion in adults and is regulated by dietary fat. The present research determined the regulation of PL by lactation and dietary fat. In Expt 1, eighteen Sprague–Dawley dams and twelve age-matched virgins (controls) were fed a low-fat diet (LF; 11 % energy as safflower oil) for 7–63 d. At postpartum (day 0), peak lactation (day 15) and post-lactation (day 56) and after 7 d in virgins, the pancreas was removed for mRNA and enzyme analyses. In Expt 2, thirty-six Sprague–Dawley dams were fed LF until day 9 postpartum when dams were divided into three groups of twelve; one continued to be fed LF, one was fed a moderate-fat diet (MF; 40 % energy as safflower oil); and one was fed a high-fat diet (HF; 67 % energy as safflower oil) diet. At peak lactation (day 15) and post-lactation (day 56), the pancreas was removed for mRNA and enzyme analyses. Expt 1 revealed that lactation and post-lactation significantly (P<0·001) decreased PL mRNA (67 % and 76 %, respectively), but only post-lactation decreased PL activity. Increased dietary fat in Expt 2 significantly increased PL mRNA (LF<MF<HF, P<0·001) and PL activity (LF<MF=HF, P<0·02) in both lactation and post-lactation. In summary, lactation and post-lactation decreased PL mRNA significantly even though dietary fat still regulated PL activity and mRNA in lactation and post-lactation.


2011 ◽  
Vol 52 (5) ◽  
pp. 982-990 ◽  
Author(s):  
Xunjun Xiao ◽  
Leah E. Ross ◽  
Rita A. Miller ◽  
Mark E. Lowe

Author(s):  
B SIAS ◽  
F FERRATO ◽  
M PELLICERRUBIO ◽  
Y FORGERIT ◽  
P GUILLOUET ◽  
...  

1997 ◽  
Vol 273 (2) ◽  
pp. G374-G380 ◽  
Author(s):  
J. Borovicka ◽  
W. Schwizer ◽  
C. Mettraux ◽  
C. Kreiss ◽  
B. Remy ◽  
...  

Gastric lipase (HGL) contributes significantly to fat digestion. However, little is known about its neurohormonal regulation in humans. We studied the role of CCK and cholinergic mechanisms in the postprandial regulation of HGL and pancreatic lipase (HPL) secretion in six healthy subjects. Gastric emptying of a mixed meal and outputs of HGL, pepsin, acid, and HPL were determined with a double-indicator technique. Three experiments were performed in random order: intravenous infusion of 1) placebo, 2) low-dose atropine (5 micrograms.kg-.h-1), and 3) the CCK-A receptor antagonist loxiglumide (22 mumol.kg-.h-1). Atropine decreased postprandial outputs of HGL, pepsin, gastric acid, and HPL (P < 0.03) while slowing gastric emptying (P < 0.05). Loxiglumide markedly increased the secretion of HGL, pepsin, and acid while distinctly reducing HPL outputs and accelerating gastric emptying (P < 0.03). Plasma CCK and gastrin levels increased during loxiglumide infusion (P < 0.03). Atropine enhanced gastrin but not CCK release. Postprandial HGL, pepsin, and acid secretion are under positive cholinergic but negative CCK control, whereas HPL is stimulated by cholinergic and CCK mechanisms. We conclude that CCK and cholinergic mechanisms have an important role in the coordination of HGL and HPL secretion to optimize digestion of dietary lipids in humans.


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