Publications by authors named "Susanne Hede"

Article Synopsis
  • The study examines how growth patterns from fetal development to infancy impact the likelihood of childhood overweight, focusing on the first 1000 days from conception to age two.
  • Analyzing data from over 6200 children, researchers identified three growth patterns: average, accelerated, and decelerated, finding that accelerated infant growth significantly increases odds of being overweight later on.
  • The findings suggest that both fetal and infant growth independently influence the risk of overweight, with specific growth combinations showing varying effects on this association.
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Introduction: Several evaluations of lifestyle interventions for childhood obesity exist; however, follow-up beyond 2 years is necessary to validate the effect. The aim of the present study was to investigate long-term weight development following children participating in one of two pragmatic family-centered lifestyle interventions treating childhood obesity.

Methods: This real-life observational study included Danish children 4-17 years of age classified as having obesity.

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Context: Children of women with gestational diabetes (GDM) are often born with a higher birthweight and have an increased risk of overweight during childhood. High fetal growth rate is also associated with being overweight in childhood.

Objective: To examine excessive fetal growth rate as a mediator between GDM and overweight in the offspring.

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Potassium channels play a vital role in maintaining the membrane potential and the driving force for anion secretion in epithelia. In pancreatic ducts, which secrete bicarbonate-rich fluid, the identity of K(+) channels has not been extensively investigated. In this study, we investigated the molecular basis of functional K(+) channels in rodent and human pancreatic ducts (Capan-1, PANC-1, and CFPAC-1) using molecular and electrophysiological techniques.

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Pancreas secretes fluid rich in digestive enzymes and bicarbonate. The alkaline secretion is important in buffering of acid chyme entering duodenum and for activation of enzymes. This secretion is formed in pancreatic ducts, and studies to date show that plasma membranes of duct epithelium express H(+)/HCO(3)(-) transporters, which depend on gradients created by the Na(+)/K(+)-ATPase.

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Previously, we have shown that pancreatic acini release adenosine triphosphate (ATP) and ATP-handling enzymes, and pancreatic ducts express various purinergic P2 receptors. The aim of the present study was to establish whether pancreatic ducts also express adenosine receptors and whether these could be involved in secretory processes, which involve cystic fibrosis transmembrane regulator (CFTR) Cl- channels or Ca2+-activated Cl- channels and H(+)/HCO(-)(3) transporters. Reverse transcriptase polymerase chain reaction analysis on rat pancreatic ducts and human duct cell adenocarcinoma lines showed that they express A1, A2A, A2B, and A3 receptors.

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The general phosphate need in mammalian cells is accommodated by members of the P(i) transport (PiT) family (SLC20), which use either Na(+) or H(+) to mediate inorganic phosphate (P(i)) symport. The mammalian PiT paralogs PiT1 and PiT2 are Na(+)-dependent P(i) (NaP(i)) transporters and are exploited by a group of retroviruses for cell entry. Human PiT1 and PiT2 were characterized by expression in Xenopus laevis oocytes with (32)P(i) as a traceable P(i) source.

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Extracellular ATP is an important regulator of transepithelial transport in a number of tissues. In pancreatic ducts, we have shown that ATP modulates epithelial K+ channels via purinergic receptors, most likely the P2Y2 and P2Y4 receptors, but the identity of the involved K+ channels was not clear. In this study, we show by RT-PCR analysis that rat pancreatic ducts express Ca(2+)-activated K+ channels of intermediate conductance (IK) and big conductance (BK), but not small conductance (SK).

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