Impaired Phosphate Tolerance Revealed With An Acute Oral Challenge

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Impaired Phosphate Tolerance Revealed With an Acute Oral

Impaired Phosphate Tolerance Revealed With an Acute Oral Challenge Mandy E Turner,1 Christine A White,2 Wilma M Hopman,3,4 Emilie C Ward,1 Paul S Jeronimo,1 Michael A Adams,1 and Rachel M Holden1,2 1Department of Biomedical and Molecular Science, Queen s University, Kingston, Canada 2Department of Medicine, Queen s University, Kingston, Canada

Acute dietary fat intake initiates alterations in energy

volunteers (Figure 1 and Table 1) received either an oral dose of PO (~1.18 g/kg BW) or an identical volume of VCL on 2 occasions in random order, spaced by an 8-week interval. Figure 1. CONSORT flow diagram. Forty-four patients underwent screening, which included a medical history, BMI analyses, and bioimpedance and an oral glucose tolerance

Sleep duration and quality as related to left ventricular

Impaired phosphate tolerance revealed with an acute oral challenge. Turner ME, White CA, Hopman WM, Ward EC, Jeronimo PS, Adams MA, Holden RM. J Bone Miner Res. 2017 Sep 15. doi: 10.1002/jbmr.3294. [Epub ahead of print] PMID: 28914962 Uric acid association with pulsatile and steady components of central and peripheral blood pressures.

Acaaddemmiicc Sccii eenncess International Journal of

Objective: To evaluate the acute effect of single doses of benfotiamine and silibinin on postprandial hyperglycaemia after sucrose challenge in healthy subjects. Methods: Thirteen normal healthy subjects with normal glucose tolerance were enrolled in an open label, crossover study. Theyreceived5 types of


The glucose-6-phosphate of the cell could then be built up into glycogen or metabolized by three separate pathways-by the Emden-Meyerhof route to carbon dioxide and water, by the pentose phosphate route to produce a source of reduced co-enzyme II, or by the uronate pathway producing glucuronic acid. The pentose source of co-enzyme II was

Hyperinsulinemia, glucose intolerance, and dyslipidemia

increase in blood glucose concentration in response to oral glucose intake. The increases in both glycogen and glucose 6-phosphate content, as well as in Akt and glycogen synthase activities in the liver, that were induced by glucose intake were markedly impaired in mice expressing Δp85. Despite an upregulation of mRNAs for gluconeogenic enzymes

Chapter II - Introduction 2.1. Historic retrospective of Diabetes

higher than those considered normal. These people were defined as having impaired fasting glucose (IFG) when IFG levels vary from 100 mg/dL (5.6 mmol/L) to 125 mg/dL (6.9 mmol/L), or impaired glucose tolerance (IGT) when 2-h values in the oral glucose tolerance test (OGTT) are between 140 mg/dL (7.8 mmol/L) to 199 mg/dL (11.0

Unusual presentation of more common disease/injury Coeliac

levels, oral calcium supplementation is sufficient. In the acute management of severe hypocalcaemia associated with coeliac disease, it is important to identify other pos-sible factors, in addition to malabsorption, which might be contributing to the hypocalcaemia. Coeliac disease may cause hypomagnesemic hypocalcaemia and

The Role of SIRT1 in Pancreatic Beta Cells

knockout mouse model (Sirt1BKO), oral glucose challenge revealed a glucose intolerant phenotype with reduced insulin secretion. Isolated Sirt1BKO islets also secreted less insulin without changes to insulin content or islet morphology. Intracellular defects were localized to the mitochondria and showed suppressed bioenergetics negatively

Summary and general discussion

Summary and general discussion expressed by epithelial cells at portes d entrees and macrophages play a role in the second line of defense, these cells were used to investigate in Chapter 2 the capacity