Results 121 to 130 of about 17,404,319 (246)
Diabetes, Obesity and Metabolism, EarlyView.ABSTRACT Aims/Hypothesis Glucose‐dependent insulinotropic polypeptide (GIP) is a bidirectional glucose‐stabilising hormone potentiating insulin secretion at high glucose levels and glucagon secretion during normal‐to‐low plasma glucose levels. Preclinically, GIP and the amino acid alanine show synergistic glucagonotropic effects at low glucose levels ...
Julie Warnøe +13 more
wiley +1 more source
New insights in pediatric metabolic medicine: pathogenesis of cholesterol biosynthesis defects and innovative therapies for Pompe disease [PDF]
, 2007 Rossi, Emiliano
core +1 more source
Orphanet Journal of Rare DiseasesBackground Late-onset Pompe disease (LOPD) is a rare inherited genetic condition caused by deficiency of acid α-glucosidase (GAA) and accumulation of lysosomal glycogen.
Mark Corbett +9 more
doaj +1 more source
Entomologia Experimentalis et Applicata, EarlyView.Using DNA metabarcoding, this study investigates pollen transported by syrphids (Syrphidae) in the Dolomiti Bellunesi National Park and agricultural sites in Northern Italy. The analysis reveals a high diversity of visited plant taxa, including previously undocumented plant–pollinator interactions.
Serena Magagnoli +6 more
wiley +1 more source
A New Mutation Causing Severe Infantile-Onset Pompe Disease Responsive to Enzyme Replacement Therapy
Iranian Journal of Medical Sciences, 2018 Pompe disease (PD), also known as “glycogen storage disease type II (OMIM # 232300)” is a rare autosomal recessive disorder characterized by progressive glycogen accumulation in cellular lysosomes. It ultimately leads to cellular damage.
Hossein Moravej +5 more
doaj
Enzyme replacement therapy during pregnancy and breastfeeding in late-onset Pompe disease
International Breastfeeding JournalBackground Pompe disease is an autosomal recessively inherited lysosomal storage disorder, caused by enzyme deficiency of acid alpha-glucosidase (GAA). This deficiency leads to the accumulation of glycogen in lysosomes and subsequent muscle dysfunction ...
Magdalena Bachmann +7 more
doaj +1 more source
CD36‐mediated lipid rewiring in the metabolic adaptation of tumour ecosystems
The FEBS Journal, EarlyView.Nutrient deprivation drives a lipid‐centric shift in tumour metabolic symbiosis and signalling network. CD36 functions as a bidirectional bridge, transferring fatty acids from stromal donors (adipocytes, CAFs) to the ecosystem tumour‐ and microenvironment‐dependently.
Anna Sebestyén +11 more
wiley +1 more source
Nursing care about child with glycogen storage disease I. type
, 2018 Present Situation: Research investigation deals with nursing care of the child with glycogen storage disease type I., as well as its diagnosis, nutritional management and complications.
ŠŤASTNÍKOVÁ, Hana
core
Pregnancies and associated events in women receiving Enzyme Replacement Therapy for late onset Glycogen Storage Disease Type II (Pompe disease) [PDF]
, 2016 AIM: Glycogen storage disease type II (GSD II or Pompe disease; OMIM; 232 300) is a rare autosomal recessive lysosomal storage disorder resulting from deficiency of α-glucosidase and accumulation of glycogen in muscle.
Rohman, PJ +4 more
core
Tankyrase‐2 regulates adipocyte differentiation through AMPK/mTOR signaling
The FEBS Journal, EarlyView.Tankyrase 2 (TNKS2), a PARP family member, underpins adipocyte differentiation. TNKS2 controls LKB1 protein level, and consequently, the activity of the mTOR/AMPK system and adipocyte differentiation through a layered process. Pharmacological inhibition of TNKS2 leaves other PARPs and DNA repair active and therefore represents a novel target in ...
Boglarka Rauch +7 more
wiley +1 more source