scholarly journals Variation in insulin response to oral sugar test in a cohort of horses throughout the year and evaluation of risk factors for insulin dysregulation

2021 ◽  
Author(s):  
Ninja P. Karikoski ◽  
Justin R. Box ◽  
Anna K. Mykkänen ◽  
Veikko V. Kotiranta ◽  
Marja R. Raekallio

2006 ◽  
Vol 257 ◽  
pp. 1-3 ◽  

In a nutshellGrapefruit can prolong the half life of various drugs, such as statins and benzodiapenes.There is also reason to believe that grapefruit - either as juice or the whole fruit - has potential to lower cancer risk, improve insulin response and cardiovascular risk factors, and possibly even help lose weight.



PeerJ ◽  
2021 ◽  
Vol 9 ◽  
pp. e10764
Author(s):  
Julien Delarocque ◽  
Florian Frers ◽  
Korinna Huber ◽  
Klaus Jung ◽  
Karsten Feige ◽  
...  

Background Insulin dysregulation (ID) is an equine endocrine disorder, which is often accompanied by obesity and various metabolic perturbations. The relationship between weight variations and fluctuations of the insulin response to oral glucose tests (OGT) as well as the metabolic impact of ID have been described previously. The present study seeks to characterize the concomitant metabolic impact of variations in the insulin response and bodyweight during repeated OGTs using a metabolomics approach. Methods Nineteen Icelandic horses were subjected to five OGTs over one year and their bodyweight, insulin and metabolic response were monitored. Analysis of metabolite concentrations depending on time (during the OGT), relative bodyweight (rWeight; defined as the bodyweight at one OGT divided by the mean bodyweight across all OGTs) and relative insulin response (rAUCins; defined accordingly from the area under the insulin curve during OGT) was performed using linear models. Additionally, the pathways significantly associated with time, rWeight and rAUCins were identified by rotation set testing. Results The results suggested that weight gain and worsening of ID activate distinct metabolic pathways. The metabolic profile associated with weight gain indicated an increased activation of arginase, while the pathways associated with time and rAUCins were consistent with the expected effect of glucose and insulin, respectively. Overall, more metabolites were significantly associated with rWeight than with rAUCins.



2017 ◽  
Vol 88 (3-4) ◽  
pp. 265-273 ◽  
Author(s):  
Christiane S. Hampe ◽  
Michele L. Shaffer ◽  
Christian L. Roth

Background: Obesity is strongly associated with insulin resistance, hypertension, dyslipidemia, and therefore risk for metabolic syndrome (MetS), which is an increasing problem in youth. The potential role of elevated liver enzyme levels in this context needs to be further investigated. Methods: This paper provides a post hoc analysis of a cross-sectional study of 77 obese nondiabetic children (51% female; median age 11.7 years; BMI >97th percentile) enrolled at the University of Bonn, Bonn, Germany. Anthropometric parameters, lipid profiles, glycemic control, and liver enzyme levels were evaluated. Glucose and insulin levels were determined during an oral glucose tolerance test (OGTT). Gender- and age-specific cutoff values were used to assess MetS. Results: A high prevalence of hypertension (51%), dyslipidemia (52%), elevated liver enzyme levels (51%), and hyperglycemia (24%) was found. There was considerable overlap between the presence of different MetS risk factors in individuals, and 40% of the participants had ≥3 of a maximum of 5 MetS risk factors. Elevated liver enzyme levels were significantly associated with reduced insulin sensitivity, as the OGTT-insulin response was significantly higher in participants with elevated transaminases (p = 0.01). This association was independent of hyperglycemia and dyslipidemia (p = 0.03). Conclusions: We conclude that liver enzyme levels are related to insulin sensitivity in obese children and could therefore be an indirect indicator for MetS. Testing for disturbed glucose metabolism should be considered for obese children with elevated liver enzymes.



PeerJ ◽  
2018 ◽  
Vol 6 ◽  
pp. e4316 ◽  
Author(s):  
Murad H. Kheder ◽  
Simon R. Bailey ◽  
Kevin J. Dudley ◽  
Martin N. Sillence ◽  
Melody A. de Laat

Background Equine metabolic syndrome (EMS) is associated with insulin dysregulation, which often manifests as post-prandial hyperinsulinemia. Circulating concentrations of the incretin hormone, glucagon-like peptide-1 (GLP-1) correlate with an increased insulin response to carbohydrate intake in animals with EMS. However, little is known about the equine GLP-1 receptor (eGLP-1R), or whether GLP-1 concentrations can be manipulated. The objectives were to determine (1) the tissue localisation of the eGLP-1R, (2) the GLP-1 secretory capacity of equine intestine in response to glucose and (3) whether GLP-1 stimulated insulin secretion from isolated pancreatic islets can be attenuated. Methods Archived and abattoir-sourced tissues from healthy horses were used. Reverse transcriptase PCR was used to determine the tissue distribution of the eGLP-1R gene, with immunohistochemical confirmation of its pancreatic location. The GLP-1 secretion from intestinal explants in response to 4 and 12 mM glucose was quantified in vitro. Pancreatic islets were freshly isolated to assess the insulin secretory response to GLP-1 agonism and antagonism in vitro, using concentration-response experiments. Results The eGLP-1R gene is widely distributed in horses (pancreas, heart, liver, kidney, duodenum, digital lamellae, tongue and gluteal skeletal muscle). Within the pancreas the eGLP-1R was immunolocalised to the pancreatic islets. Insulin secretion from pancreatic islets was concentration-dependent with human GLP-1, but not the synthetic analogue exendin-4. The GLP-1R antagonist exendin 9-39 (1 nM) reduced (P = 0.08) insulin secretion by 27%. Discussion The distribution of the eGLP-1R across a range of tissues indicates that it may have functions beyond insulin release. The ability to reduce insulin secretion, and therefore hyperinsulinemia, through eGLP-1R antagonism is a promising and novel approach to managing equine insulin dysregulation.



1987 ◽  
Vol 5 (1-2) ◽  
pp. 9-17 ◽  
Author(s):  
Norman J. Blacklock

Idiopathic renal stone comprises more than SO per cent of kidney stone disease. Whilst the incidence rate in the Western World is high, that in Africa south of the Sahara is very low. Epidemiological studies point to a dietary aetiology as the basis for stone formation in the kidney. A number of dietary constituents increase the urinary risk factors for stone formation and one of these is sucrose. The sucrose effect is exaggerated when it is consumed in certain forms. There is also the evidence that a third of a normal population responds in an exaggerated manner in respect of an increased excretion of urinary risk factors when sucrose is consumed and this phenomenon has been noted in over 70 per cent of idiopathic stone formers. In studying the mechanism of this, insulin was found to influence distal renal tubular function to increased calcium excretion. Stone formers with an exaggerated urinary risk factor response to sucrose were found to have abnormally high and sustained blood levels of insulin following a standard glucose test meal. Where sucrose or sucrose products are in abundance, quite apart from its effect in increasing urinary risk factors in the population in general, there is particular vulnerability of a significant sub group within the population with this type of insulin response. Sucrose furthermore is known to induce nephrocalcinosis in the kidney of the rodent and similar calcific lesions have been found in the kidney substance of man and these have been observed to begin to appear within the first decade of life. Sucrose has also been observed in man to increase the excretion rate of an enzyme which is identified with renal tubular cell damage.



2019 ◽  
Vol 133 (22) ◽  
pp. 2283-2299
Author(s):  
Apabrita Ayan Das ◽  
Devasmita Chakravarty ◽  
Debmalya Bhunia ◽  
Surajit Ghosh ◽  
Prakash C. Mandal ◽  
...  

Abstract The role of inflammation in all phases of atherosclerotic process is well established and soluble TREM-like transcript 1 (sTLT1) is reported to be associated with chronic inflammation. Yet, no information is available about the involvement of sTLT1 in atherosclerotic cardiovascular disease. Present study was undertaken to determine the pathophysiological significance of sTLT1 in atherosclerosis by employing an observational study on human subjects (n=117) followed by experiments in human macrophages and atherosclerotic apolipoprotein E (apoE)−/− mice. Plasma level of sTLT1 was found to be significantly (P<0.05) higher in clinical (2342 ± 184 pg/ml) and subclinical cases (1773 ± 118 pg/ml) than healthy controls (461 ± 57 pg/ml). Moreover, statistical analyses further indicated that sTLT1 was not only associated with common risk factors for Coronary Artery Disease (CAD) in both clinical and subclinical groups but also strongly correlated with disease severity. Ex vivo studies on macrophages showed that sTLT1 interacts with Fcɣ receptor I (FcɣRI) to activate spleen tyrosine kinase (SYK)-mediated downstream MAP kinase signalling cascade to activate nuclear factor-κ B (NF-kB). Activation of NF-kB induces secretion of tumour necrosis factor-α (TNF-α) from macrophage cells that plays pivotal role in governing the persistence of chronic inflammation. Atherosclerotic apoE−/− mice also showed high levels of sTLT1 and TNF-α in nearly occluded aortic stage indicating the contribution of sTLT1 in inflammation. Our results clearly demonstrate that sTLT1 is clinically related to the risk factors of CAD. We also showed that binding of sTLT1 with macrophage membrane receptor, FcɣR1 initiates inflammatory signals in macrophages suggesting its critical role in thrombus development and atherosclerosis.





2011 ◽  
Vol 21 (2) ◽  
pp. 59-62
Author(s):  
Joseph Donaher ◽  
Christina Deery ◽  
Sarah Vogel

Healthcare professionals require a thorough understanding of stuttering since they frequently play an important role in the identification and differential diagnosis of stuttering for preschool children. This paper introduces The Preschool Stuttering Screen for Healthcare Professionals (PSSHP) which highlights risk factors identified in the literature as being associated with persistent stuttering. By integrating the results of the checklist with a child’s developmental profile, healthcare professionals can make better-informed, evidence-based decisions for their patients.



2010 ◽  
Vol 20 (3) ◽  
pp. 76-83 ◽  
Author(s):  
Joseph Donaher ◽  
Tom Gurrister ◽  
Irving Wollman ◽  
Tim Mackesey ◽  
Michelle L. Burnett

Parents of children who stutter and adults who stutter frequently ask speech-language pathologists to predict whether or not therapy will work. Even though research has explored risk-factors related to persistent stuttering, there remains no way to determine how an individual will react to a specific therapy program. This paper presents various clinicians’answers to the question, “What do you tell parents or adults who stutter when they ask about cure rates, outcomes, and therapy efficacy?”



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