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  1. AU="Rory J McCrimmon"
  2. AU="Ahdoot, Aaron I."
  3. AU="Neote, Kuldeep S"
  4. AU="Shen, Congcong"
  5. AU="Rahi, Kosar"
  6. AU="Channabasavaiah, Jagadish Puralae"
  7. AU="Anselmi, Maurizio"
  8. AU="Chauhan, D."
  9. AU="Nicoll, Roger A"
  10. AU="Kwon, Young-Sam"
  11. AU="Mihwa Lee"
  12. AU="Yuanting Jin"
  13. AU="Ter Haar, Eva"
  14. AU="Wolin, Dan L"
  15. AU="Zhang, Tenan"
  16. AU="Piedrafita, Lídia"
  17. AU="Nandy, Ananya"
  18. AU="Bansemer, Sven"
  19. AU="Kochetov, O"
  20. AU="Liu, Fen"

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  1. Artikel ; Online: Central deficiency of IL-6Ra in mice impairs glucose-stimulated insulin secretion

    Alison D. McNeilly / Adonis Yianakas / Jennifer G. Gallagher / Jamie Tarlton / Michael LJ. Ashford / Rory J. McCrimmon

    Molecular Metabolism, Vol 61, Iss , Pp 101488- (2022)

    2022  

    Abstract: Objective: IL-6 is an important contributor to glucose and energy homeostasis through changes in whole-body glucose disposal, insulin sensitivity, food intake and energy expenditure. However, the relative contributions of peripheral versus central IL-6 ... ...

    Abstract Objective: IL-6 is an important contributor to glucose and energy homeostasis through changes in whole-body glucose disposal, insulin sensitivity, food intake and energy expenditure. However, the relative contributions of peripheral versus central IL-6 signaling to these metabolic actions are presently unclear. A conditional mouse model with reduced brain IL-6Ra expression was used to explore how blunted central IL-6 signaling alters metabolic status in lean and obese mice. Methods: Transgenic mice with reduced levels of central IL-6 receptor alpha (IL-6Ra) (IL-6Ra KD mice) and Nestin Cre controls (Cre+/- mice) were fed standard chow or high-fat diet for 20 weeks. Obese and lean mouse cohorts underwent metabolic phenotyping with various measures of energy and glucose homeostasis determined. Glucose-stimulated insulin secretion was assessed in vivo and ex vivo in both mouse groups. Results: IL-6Ra KD mice exhibited altered body fat mass, liver steatosis, plasma insulin, IL-6 and NEFA levels versus Cre+/- mice in a diet-dependent manner. IL-6Ra KD mice had increased food intake, higher RER, decreased energy expenditure with diminished cold tolerance compared to Cre+/- controls. Standard chow-fed IL-6Ra KD mice displayed reduced plasma insulin and glucose-stimulated insulin secretion with impaired glucose disposal and unchanged insulin sensitivity. Isolated pancreatic islets from standard chow-fed IL-6Ra KD mice showed comparable morphology and glucose-stimulated insulin secretion to Cre+/- controls. The diminished in vivo insulin secretion exhibited by IL-6Ra KD mice was recovered by blockade of autonomic ganglia. Conclusions: This study shows that central IL-6Ra signaling contributes to glucose and energy control mechanisms by regulating food intake, energy expenditure, fuel flexibility and insulin secretion. A plausible mechanism linking central IL-6Ra signaling and pancreatic insulin secretion is through the modulation of autonomic output activity. Thus, brain IL-6 signaling may contribute to the central ...
    Schlagwörter Interleukin-6 ; Food intake ; Energy expenditure ; Insulin secretion ; Autonomic output ; Internal medicine ; RC31-1245
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2022-07-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  2. Artikel ; Online: Metformin increases the uptake of glucose into the gut from the circulation in high-fat diet-fed male mice, which is enhanced by a reduction in whole-body Slc2a2 expression

    Nicola Morrice / Susanne Vainio / Kirsi Mikkola / Lidy van Aalten / Jennifer R. Gallagher / Michael L.J. Ashford / Alison D. McNeilly / Rory J. McCrimmon / Alexandra Grosfeld / Patricia Serradas / Jukka Koffert / Ewan R. Pearson / Pirjo Nuutila / Calum Sutherland

    Molecular Metabolism, Vol 77, Iss , Pp 101807- (2023)

    2023  

    Abstract: Objectives: Metformin is the first line therapy recommended for type 2 diabetes. However, the precise mechanism of action remains unclear and up to a quarter of patients show some degree of intolerance to the drug, with a similar number showing poor ... ...

    Abstract Objectives: Metformin is the first line therapy recommended for type 2 diabetes. However, the precise mechanism of action remains unclear and up to a quarter of patients show some degree of intolerance to the drug, with a similar number showing poor response to treatment, limiting its effectiveness. A better understanding of the mechanism of action of metformin may improve its clinical use. SLC2A2 (GLUT2) is a transmembrane facilitated glucose transporter, with important roles in the liver, gut and pancreas. Our group previously identified single nucleotide polymorphisms in the human SLC2A2 gene, which were associated with reduced transporter expression and an improved response to metformin treatment. The aims of this study were to model Slc2a2 deficiency and measure the impact on glucose homoeostasis and metformin response in mice. Methods: We performed extensive metabolic phenotyping and 2-deoxy-2-[18F]fluoro-d-glucose ([18F]FDG)-positron emission tomography (PET) analysis of gut glucose uptake in high-fat diet-fed (HFD) mice with whole-body reduced Slc2a2 (Slc2a2+/−) and intestinal Slc2a2 KO, to assess the impact of metformin treatment. Results: Slc2a2 partial deficiency had no major impact on body weight and insulin sensitivity, however mice with whole-body reduced Slc2a2 expression (Slc2a2+/−) developed an age-related decline in glucose homoeostasis (as measured by glucose tolerance test) compared to wild-type (Slc2a2+/+) littermates. Glucose uptake into the gut from the circulation was enhanced by metformin exposure in Slc2a2+/+ animals fed HFD and this action of the drug was significantly higher in Slc2a2+/− animals. However, there was no effect of specifically knocking-out Slc2a2 in the mouse intestinal epithelial cells. Conclusions: Overall, this work identifies a differential metformin response, dependent on expression of the SLC2A2 glucose transporter, and also adds to the growing evidence that metformin efficacy includes modifying glucose transport in the gut. We also describe a novel and important ...
    Schlagwörter Diabetes ; Metformin ; Slc2a2 ; Glucose-uptake ; [18F]FDG-PET ; Internal medicine ; RC31-1245
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2023-11-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  3. Artikel ; Online: Impaired counter-regulatory and symptomatic responses to hypoglycemia in type 1 diabetes

    Rory J McCrimmon

    Diabetic Hypoglycemia, Vol 4, Iss 1, Pp 3-

    underlying mechanisms

    2011  Band 7

    Abstract: Hypoglycemia is recognized as the principal limitation to intensive insulin therapy and is associated with potential long-term physical and psychological morbidity as well as a recognized mortality. This feature article describes the primary defects in ... ...

    Abstract Hypoglycemia is recognized as the principal limitation to intensive insulin therapy and is associated with potential long-term physical and psychological morbidity as well as a recognized mortality. This feature article describes the primary defects in glucose counter-regulation that are almost universally present in individuals with type 1 diabetes and are responsible for the increased frequency of hypoglycemia, as well as briefly discusses the current state of research into the more basic mechanisms underlying the detection of hypoglycemia. The mechanisms that lead to defective counter-regulation in type 1 diabetes are also highlighted, particularly those resulting from repeated hypoglycemia, and the effectiveness or validity of therapies designed to restore hypoglycemia counter-regulation. Improved understanding of the mechanisms that contribute to defective hypoglycemia counter-regulation will help guide our attempts to intervene therapeutically and prevent this distressing complication of insulin treatment.
    Schlagwörter diabetic hypoglycemia ; Diseases of the endocrine glands. Clinical endocrinology ; RC648-665 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Internal medicine ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
    Thema/Rubrik (Code) 610
    Sprache Englisch
    Erscheinungsdatum 2011-06-01T00:00:00Z
    Verlag ESP Bioscience
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  4. Artikel ; Online: The complex interplay between hypoglycemia and exercise

    Rory J McCrimmon

    Diabetic Hypoglycemia, Vol 4, Iss 2, Pp 1-

    2011  Band 2

    Schlagwörter diabetic hypoglycemia ; Diseases of the endocrine glands. Clinical endocrinology ; RC648-665 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Internal medicine ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
    Sprache Englisch
    Erscheinungsdatum 2011-10-01T00:00:00Z
    Verlag ESP Bioscience
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  5. Artikel ; Online: Investigating the day-to-day impact of hypoglycaemia in adults with type 1 or type 2 diabetes

    Giesje Nefs / Frans Pouwer / Alan Brennan / Pratik Choudhary / Jane Speight / Ulrik Pedersen-Bjergaard / Christel Hendrieckx / Daniel John Pollard / Rory J McCrimmon / Melanie Broadley / Bastiaan de Galan / Uffe Søholm / Natalie Zaremba / Patrick Divilly / Zeinab Mahmoudi / Stephanie A. Amiel

    BMJ Open, Vol 12, Iss

    design and validation protocol of the Hypo-METRICS application

    2022  Band 2

    Schlagwörter Medicine ; R
    Sprache Englisch
    Erscheinungsdatum 2022-02-01T00:00:00Z
    Verlag BMJ Publishing Group
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  6. Artikel ; Online: In-vivo correlations between skin metabolic oscillations and vasomotion in wild-type mice and in a model of oxidative stress

    Salvatore Smirni / Alison D. McNeilly / Michael P. MacDonald / Rory J. McCrimmon / Faisel Khan

    Scientific Reports, Vol 9, Iss 1, Pp 1-

    2019  Band 15

    Abstract: Abstract Arterioles in the cutaneous microcirculation frequently display an oscillatory phenomenon defined vasomotion, consistent with periodic diameter variations in the micro-vessels associated with particular physiological or abnormal conditions. The ... ...

    Abstract Abstract Arterioles in the cutaneous microcirculation frequently display an oscillatory phenomenon defined vasomotion, consistent with periodic diameter variations in the micro-vessels associated with particular physiological or abnormal conditions. The cellular mechanisms underlying vasomotion and its physiological role have not been completely elucidated. Various mechanisms were demonstrated, based on cell Ca2+ oscillations determined by the activity of channels in the plasma membrane or sarcoplasmic reticulum of vascular cells. However, the possible engagement in vasomotion of cell metabolic oscillations of mitochondrial or glycolytic origin has been poorly explored. Metabolic oscillations associated with the production of ATP energy were previously described in cells, while limited studies have investigated these fluctuations in-vivo. Here, we characterised a low-frequency metabolic oscillator (MO-1) in skin from live wild-type and Nrf2−/− mice, by combination of fluorescence spectroscopy and wavelet transform processing technique. Furthermore, the relationships between metabolic and microvascular oscillators were examined during phenylephrine-induced vasoconstriction. We found a significant interaction between MO-1 and the endothelial EDHF vasomotor mechanism that was reduced in the presence of oxidative stress (Nrf2−/− mice). Our findings suggest indirectly that metabolic oscillations may be involved in the mechanisms underlying endothelium-mediated skin vasomotion, which might be altered in the presence of metabolic disturbance.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2019-01-01T00:00:00Z
    Verlag Nature Publishing Group
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  7. Artikel ; Online: Adipocyte integrin-linked kinase plays a key role in the development of diet-induced adipose insulin resistance in male mice

    Aimée R. Bugler-Lamb / Annie Hasib / Xiong Weng / Chandani K. Hennayake / Chenshi Lin / Rory J. McCrimmon / Roland H. Stimson / Michael L.J. Ashford / David H. Wasserman / Li Kang

    Molecular Metabolism, Vol 49, Iss , Pp 101197- (2021)

    2021  

    Abstract: Objective: Increased deposition of the extracellular matrix (ECM) in adipose tissue (AT) during obesity contributes to insulin resistance. The integrin receptors transmit changes in the extracellular environment causing corresponding intracellular ... ...

    Abstract Objective: Increased deposition of the extracellular matrix (ECM) in adipose tissue (AT) during obesity contributes to insulin resistance. The integrin receptors transmit changes in the extracellular environment causing corresponding intracellular adaptations. Integrin-linked kinase (ILK), an adaptor protein, is a central hub for intracellular signaling of integrins. This study determined the role of ILK in adipose function and insulin resistance. Methods: The pathogenic role of ILK in obesity and insulin resistance was studied in human adipose tissue and adipocyte-specific ILK-deficient mice (ILKlox/loxAdCre). ILKlox/loxAdCre mice together with wild-type littermates (ILKlox/lox) were fed a chow diet or 60% high-fat (HF) diet for 16 weeks. In vivo insulin sensitivity was determined by hyperinsulinemic-euglycemic clamps. Results: AT ILK expression was increased by HF diet feeding in mice and increased in visceral fat of morbidly obese humans. The HF-fed ILKlox/loxAdCre mice displayed reduced fat mass and improved glucose tolerance relative to the HF-fed ILKlox/lox mice. During a hyperinsulinemic-euglycemic clamp, the HF-fed ILKlox/loxAdCre mice exhibited partially improved insulin resistance in AT. Lipolysis was suppressed to a greater extent by insulin and glucose uptake in brown AT (BAT) increased. Increased inhibition of lipolysis may have been attributed to increased vascularization in white AT, while increased glucose uptake in BAT was associated with increased Akt phosphorylation and P38/JNK dephosphorylation. Notably, AT insulin sensitivity in lean mice was not affected by ILK deletion. Moreover, reduced fat mass in the HF-fed ILKlox/loxAdCre mice may have been attributed to decreased free fatty acid uptake into adipocytes via the downregulation of CD36 gene expression. Consistent with the results in the mice, knockdown and knockout of ILK in 3T3-L1 cells decreased lipid accumulation and CD36 gene expression during adipogenesis. Conclusions: These data show that adipocyte ILK is important for regulating HF ...
    Schlagwörter Adipose tissue ; Extracellular matrix ; Insulin clamp ; Insulin resistance ; Integrin-linked kinase ; Internal medicine ; RC31-1245
    Thema/Rubrik (Code) 571
    Sprache Englisch
    Erscheinungsdatum 2021-07-01T00:00:00Z
    Verlag Elsevier
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  8. Artikel ; Online: The genetic association of the transcription factor NPAT with glycemic response to metformin involves regulation of fuel selection.

    Changwei Chen / Jennifer R Gallagher / Jamie Tarlton / Lidy van Aalten / Susan E Bray / Michael L J Ashford / Rory J McCrimmon / Ewan R Pearson / Alison D McNeilly / Calum Sutherland

    PLoS ONE, Vol 16, Iss 7, p e

    2021  Band 0253533

    Abstract: The biguanide, metformin, is the first-choice therapeutic agent for type-2 diabetes, although the mechanisms that underpin metformin clinical efficacy remain the subject of much debate, partly due to the considerable variation in patient response to ... ...

    Abstract The biguanide, metformin, is the first-choice therapeutic agent for type-2 diabetes, although the mechanisms that underpin metformin clinical efficacy remain the subject of much debate, partly due to the considerable variation in patient response to metformin. Identification of poor responders by genotype could avoid unnecessary treatment and provide clues to the underlying mechanism of action. GWAS identified SNPs associated with metformin treatment success at a locus containing the NPAT (nuclear protein, ataxia-telangiectasia locus) and ATM (ataxia-telangiectasia mutated) genes. This implies that gene sequence dictates a subsequent biological function to influence metformin action. Hence, we modified expression of NPAT in immortalized cell lines, primary mouse hepatocytes and mouse tissues, and analysed the outcomes on metformin action using confocal microscopy, immunoblotting and immunocytochemistry. In addition, we characterised the metabolic phenotype of npat heterozygous knockout mice and established the metformin response following development of insulin resistance. NPAT protein was localised in the nucleus at discrete loci in several cell types, but over-expression or depletion of NPAT in immortalised cell models did not change cellular responses to biguanides. In contrast, metformin regulation of respiratory exchange ratio (RER) was completely lost in animals lacking one allele of npat. There was also a reduction in metformin correction of impaired glucose tolerance, however no other metabolic abnormalities, or response to metformin, were found in the npat heterozygous mice. In summary, we provide methodological advancements for the detection of NPAT, demonstrate that minor reductions in NPAT mRNA levels (20-40%) influence metformin regulation of RER, and propose that the association between NPAT SNPs and metformin response observed in GWAS, could be due to loss of metformin modification of cellular fuel usage.
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 570
    Sprache Englisch
    Erscheinungsdatum 2021-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  9. Artikel ; Online: Therapeutic strategies to prevent hypoglycemia using pharmacologic interventions

    Priya S George / Rory J McCrimmon

    Diabetic Hypoglycemia, Vol 5, Iss 2, Pp 13-

    2012  Band 16

    Schlagwörter diabetic hypoglycemia ; Diseases of the endocrine glands. Clinical endocrinology ; RC648-665 ; Specialties of internal medicine ; RC581-951 ; Internal medicine ; RC31-1245 ; Medicine ; R ; DOAJ:Internal medicine ; DOAJ:Medicine (General) ; DOAJ:Health Sciences
    Sprache Englisch
    Erscheinungsdatum 2012-10-01T00:00:00Z
    Verlag ESP Bioscience
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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  10. Artikel ; Online: Large socioeconomic gap in period life expectancy and life years spent with complications of diabetes in the Scottish population with type 1 diabetes, 2013-2018.

    Andreas Höhn / Stuart J McGurnaghan / Thomas M Caparrotta / Anita Jeyam / Joseph E O'Reilly / Luke A K Blackbourn / Sara Hatam / Christian Dudel / Rosie J Seaman / Joseph Mellor / Naveed Sattar / Rory J McCrimmon / Brian Kennon / John R Petrie / Sarah Wild / Paul M McKeigue / Helen M Colhoun / SDRN-Epi Group

    PLoS ONE, Vol 17, Iss 8, p e

    2022  Band 0271110

    Abstract: Background We report the first study to estimate the socioeconomic gap in period life expectancy (LE) and life years spent with and without complications in a national cohort of individuals with type 1 diabetes. Methods This retrospective cohort study ... ...

    Abstract Background We report the first study to estimate the socioeconomic gap in period life expectancy (LE) and life years spent with and without complications in a national cohort of individuals with type 1 diabetes. Methods This retrospective cohort study used linked healthcare records from SCI-Diabetes, the population-based diabetes register of Scotland. We studied all individuals aged 50 and older with a diagnosis of type 1 diabetes who were alive and residing in Scotland on 1 January 2013 (N = 8591). We used the Scottish Index of Multiple Deprivation (SIMD) 2016 as an area-based measure of socioeconomic deprivation. For each individual, we constructed a history of transitions by capturing whether individuals developed retinopathy/maculopathy, cardiovascular disease, chronic kidney disease, and diabetic foot, or died throughout the study period, which lasted until 31 December 2018. Using parametric multistate survival models, we estimated total and state-specific LE at an attained age of 50. Results At age 50, remaining LE was 22.2 years (95% confidence interval (95% CI): 21.6 - 22.8) for males and 25.1 years (95% CI: 24.4 - 25.9) for females. Remaining LE at age 50 was around 8 years lower among the most deprived SIMD quintile when compared with the least deprived SIMD quintile: 18.7 years (95% CI: 17.5 - 19.9) vs. 26.3 years (95% CI: 24.5 - 28.1) among males, and 21.2 years (95% CI: 19.7 - 22.7) vs. 29.3 years (95% CI: 27.5 - 31.1) among females. The gap in life years spent without complications was around 5 years between the most and the least deprived SIMD quintile: 4.9 years (95% CI: 3.6 - 6.1) vs. 9.3 years (95% CI: 7.5 - 11.1) among males, and 5.3 years (95% CI: 3.7 - 6.9) vs. 10.3 years (95% CI: 8.3 - 12.3) among females. SIMD differences in transition rates decreased marginally when controlling for time-updated information on risk factors such as HbA1c, blood pressure, BMI, or smoking. Conclusions In addition to societal interventions, tailored support to reduce the impact of diabetes is needed for ...
    Schlagwörter Medicine ; R ; Science ; Q
    Thema/Rubrik (Code) 360
    Sprache Englisch
    Erscheinungsdatum 2022-01-01T00:00:00Z
    Verlag Public Library of Science (PLoS)
    Dokumenttyp Artikel ; Online
    Datenquelle BASE - Bielefeld Academic Search Engine (Lebenswissenschaftliche Auswahl)

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