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  1. Article: Circadian Disruption across Lifespan Impairs Glucose Homeostasis and Insulin Sensitivity in Adult Mice.

    Her, Tracy K / Li, Jin / Lin, Hao / Liu, Dong / Root, Kate M / Regal, Jean F / Alejandro, Emilyn U / Cao, Ruifeng

    Metabolites

    2024  Volume 14, Issue 2

    Abstract: Circadian rhythm disruption is associated with impaired glucose homeostasis and type 2 diabetes. For example, night shift work is associated with an increased risk of gestational diabetes. However, the effects of chronic circadian disruption since early ... ...

    Abstract Circadian rhythm disruption is associated with impaired glucose homeostasis and type 2 diabetes. For example, night shift work is associated with an increased risk of gestational diabetes. However, the effects of chronic circadian disruption since early life on adult metabolic health trajectory remain unknown. Here, using the "Short Day" (SD) mouse model, in which an 8 h/8 h light/dark (LD) cycle was used to disrupt mouse circadian rhythms across the lifespan, we investigated glucose homeostasis in adult mice. Adult SD mice were fully entrained into the 8 h/8 h LD cycle, and control mice were entrained into the 12 h/12 h LD cycle. Under a normal chow diet, female and male SD mice displayed a normal body weight trajectory. However, female but not male SD mice under a normal chow diet displayed glucose intolerance and insulin resistance, which are associated with impaired insulin signaling/AKT in the skeletal muscle and liver. Under high-fat diet (HFD) challenges, male but not female SD mice demonstrated increased body weight gain compared to controls. Both male and female SD mice developed glucose intolerance under HFD. Taken together, these results demonstrate that environmental disruption of circadian rhythms contributes to obesity in a sexually dimorphic manner but increases the risk of glucose intolerance and insulin resistance in both males and females.
    Language English
    Publishing date 2024-02-16
    Publishing country Switzerland
    Document type Journal Article
    ZDB-ID 2662251-8
    ISSN 2218-1989
    ISSN 2218-1989
    DOI 10.3390/metabo14020126
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Pro-inflammatory β cell small extracellular vesicles induce β cell failure through activation of the CXCL10/CXCR3 axis in diabetes.

    Javeed, Naureen / Her, Tracy K / Brown, Matthew R / Vanderboom, Patrick / Rakshit, Kuntol / Egan, Aoife M / Vella, Adrian / Lanza, Ian / Matveyenko, Aleksey V

    Cell reports

    2021  Volume 36, Issue 8, Page(s) 109613

    Abstract: Coordinated communication among pancreatic islet cells is necessary for maintenance of glucose homeostasis. In diabetes, chronic exposure to pro-inflammatory cytokines has been shown to perturb β cell communication and function. Compelling evidence has ... ...

    Abstract Coordinated communication among pancreatic islet cells is necessary for maintenance of glucose homeostasis. In diabetes, chronic exposure to pro-inflammatory cytokines has been shown to perturb β cell communication and function. Compelling evidence has implicated extracellular vesicles (EVs) in modulating physiological and pathological responses to β cell stress. We report that pro-inflammatory β cell small EVs (cytokine-exposed EVs [cytoEVs]) induce β cell dysfunction, promote a pro-inflammatory islet transcriptome, and enhance recruitment of CD8
    MeSH term(s) Animals ; CD8-Positive T-Lymphocytes/immunology ; CD8-Positive T-Lymphocytes/metabolism ; Chemokine CXCL10/metabolism ; Diabetes Mellitus/pathology ; Extracellular Vesicles/metabolism ; Insulin-Secreting Cells/metabolism ; Macrophages/metabolism ; Male ; Mice, Inbred C57BL ; Receptors, CXCR3/metabolism ; Mice
    Chemical Substances Chemokine CXCL10 ; Cxcl10 protein, mouse ; Cxcr3 protein, mouse ; Receptors, CXCR3
    Language English
    Publishing date 2021-08-24
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 2649101-1
    ISSN 2211-1247 ; 2211-1247
    ISSN (online) 2211-1247
    ISSN 2211-1247
    DOI 10.1016/j.celrep.2021.109613
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Dietary carbohydrates modulate metabolic and β-cell adaptation to high-fat diet-induced obesity.

    Her, Tracy K / Lagakos, William S / Brown, Matthew R / LeBrasseur, Nathan K / Rakshit, Kuntol / Matveyenko, Aleksey V

    American journal of physiology. Endocrinology and metabolism

    2020  Volume 318, Issue 6, Page(s) E856–E865

    Abstract: Obesity is associated with several chronic comorbidities, one of which is type 2 diabetes mellitus (T2DM). The pathogenesis of obesity and T2DM is influenced by alterations in diet macronutrient composition, which regulate energy expenditure, metabolic ... ...

    Abstract Obesity is associated with several chronic comorbidities, one of which is type 2 diabetes mellitus (T2DM). The pathogenesis of obesity and T2DM is influenced by alterations in diet macronutrient composition, which regulate energy expenditure, metabolic function, glucose homeostasis, and pancreatic islet cell biology. Recent studies suggest that increased intake of dietary carbohydrates plays a previously underappreciated role in the promotion of obesity and consequent metabolic dysfunction. Thus, in this study, we utilized mouse models to test the hypothesis that dietary carbohydrates modulate energetic, metabolic, and islet adaptions to high-fat diets. To address this, we exposed C57BL/6J mice to 12 wk of 3 eucaloric high-fat diets (>60% calories from fat) with varying total carbohydrate (1-20%) and sucrose (0-20%) content. Our results show that severe restriction of dietary carbohydrates characteristic of ketogenic diets reduces body fat accumulation, enhances energy expenditure, and reduces prevailing glycemia and insulin resistance compared with carbohydrate-rich, high-fat diets. Moreover, severe restriction of dietary carbohydrates also results in functional, morphological, and molecular changes in pancreatic islets highlighted by restricted capacity for β-cell mass expansion and alterations in insulin secretory response. These studies support the hypothesis that low-carbohydrate/high-fat diets provide antiobesogenic benefits and suggest further evaluation of the effects of these diets on β-cell biology in humans.
    MeSH term(s) Adaptation, Physiological ; Adipose Tissue ; Animals ; Diabetes Mellitus, Type 2/metabolism ; Diet, Fat-Restricted ; Diet, High-Fat ; Diet, Ketogenic ; Dietary Carbohydrates ; Dietary Sucrose ; Energy Metabolism ; Glucose Tolerance Test ; Hyperglycemia/metabolism ; Insulin Resistance ; Insulin Secretion ; Insulin-Secreting Cells/metabolism ; Mice ; Obesity/metabolism
    Chemical Substances Dietary Carbohydrates ; Dietary Sucrose
    Language English
    Publishing date 2020-04-21
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 603841-4
    ISSN 1522-1555 ; 0193-1849
    ISSN (online) 1522-1555
    ISSN 0193-1849
    DOI 10.1152/ajpendo.00539.2019
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Uc I Zs.89: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  4. Article ; Online: Electrogenic sodium bicarbonate cotransporter NBCe1 regulates pancreatic β cell function in type 2 diabetes.

    Brown, Matthew R / Holmes, Heather / Rakshit, Kuntol / Javeed, Naureen / Her, Tracy K / Stiller, Alison A / Sen, Satish / Shull, Gary E / Prakash, Y S / Romero, Michael F / Matveyenko, Aleksey V

    The Journal of clinical investigation

    2021  Volume 131, Issue 17

    Abstract: Pancreatic β cell failure in type 2 diabetes mellitus (T2DM) is attributed to perturbations of the β cell's transcriptional landscape resulting in impaired glucose-stimulated insulin secretion. Recent studies identified SLC4A4 (a gene encoding an ... ...

    Abstract Pancreatic β cell failure in type 2 diabetes mellitus (T2DM) is attributed to perturbations of the β cell's transcriptional landscape resulting in impaired glucose-stimulated insulin secretion. Recent studies identified SLC4A4 (a gene encoding an electrogenic Na+-coupled HCO3- cotransporter and intracellular pH regulator, NBCe1) as one of the misexpressed genes in β cells of patients with T2DM. Thus, in the current study, we set out to test the hypothesis that misexpression of SLC4A4/NBCe1 in T2DM β cells contributes to β cell dysfunction and impaired glucose homeostasis. To address this hypothesis, we first confirmed induction of SLC4A4/NBCe1 expression in β cells of patients with T2DM and demonstrated that its expression was associated with loss of β cell transcriptional identity, intracellular alkalinization, and β cell dysfunction. In addition, we generated a β cell-selective Slc4a4/NBCe1-KO mouse model and found that these mice were protected from diet-induced metabolic stress and β cell dysfunction. Importantly, improved glucose tolerance and enhanced β cell function in Slc4a4/NBCe1-deficient mice were due to augmented mitochondrial function and increased expression of genes regulating β cell identity and function. These results suggest that increased β cell expression of SLC4A4/NBCe1 in T2DM plays a contributory role in promotion of β cell failure and should be considered as a potential therapeutic target.
    MeSH term(s) Animals ; Diabetes Mellitus, Type 2/genetics ; Diabetes Mellitus, Type 2/metabolism ; Diet, High-Fat/adverse effects ; Disease Models, Animal ; Gene Expression ; Glucose Intolerance/etiology ; Glucose Intolerance/metabolism ; Glucose Intolerance/prevention & control ; Humans ; Insulin-Secreting Cells/metabolism ; Mice ; Mice, Knockout ; Mitochondria/metabolism ; Obesity/genetics ; Obesity/metabolism ; Sodium-Bicarbonate Symporters/deficiency ; Sodium-Bicarbonate Symporters/genetics ; Sodium-Bicarbonate Symporters/metabolism ; Stress, Physiological
    Chemical Substances SLC4A4 protein, human ; Slc4a4 protein, mouse ; Sodium-Bicarbonate Symporters
    Language English
    Publishing date 2021-11-02
    Publishing country United States
    Document type Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
    ZDB-ID 3067-3
    ISSN 1558-8238 ; 0021-9738
    ISSN (online) 1558-8238
    ISSN 0021-9738
    DOI 10.1172/JCI142365
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Ua VI Zs.184: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
    ab Jg. 2022: Lesesaal (EG)

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  5. Article ; Online: Time-restricted feeding prevents deleterious metabolic effects of circadian disruption through epigenetic control of β cell function.

    Brown, Matthew R / Sen, Satish K / Mazzone, Amelia / Her, Tracy K / Xiong, Yuning / Lee, Jeong-Heon / Javeed, Naureen / Colwell, Christopher S / Rakshit, Kuntol / LeBrasseur, Nathan K / Gaspar-Maia, Alexandre / Ordog, Tamas / Matveyenko, Aleksey V

    Science advances

    2021  Volume 7, Issue 51, Page(s) eabg6856

    Abstract: Circadian rhythm disruption (CD) is associated with impaired glucose homeostasis and type 2 diabetes mellitus (T2DM). While the link between CD and T2DM remains unclear, there is accumulating evidence that disruption of fasting/feeding cycles mediates ... ...

    Abstract Circadian rhythm disruption (CD) is associated with impaired glucose homeostasis and type 2 diabetes mellitus (T2DM). While the link between CD and T2DM remains unclear, there is accumulating evidence that disruption of fasting/feeding cycles mediates metabolic dysfunction. Here, we used an approach encompassing analysis of behavioral, physiological, transcriptomic, and epigenomic effects of CD and consequences of restoring fasting/feeding cycles through time-restricted feeding (tRF) in mice. Results show that CD perturbs glucose homeostasis through disruption of pancreatic β cell function and loss of circadian transcriptional and epigenetic identity. In contrast, restoration of fasting/feeding cycle prevented CD-mediated dysfunction by reestablishing circadian regulation of glucose tolerance, β cell function, transcriptional profile, and reestablishment of proline and acidic amino acid–rich basic leucine zipper (PAR bZIP) transcription factor DBP expression/activity. This study provides mechanistic insights into circadian regulation of β cell function and corresponding beneficial effects of tRF in prevention of T2DM.
    Language English
    Publishing date 2021-12-15
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2810933-8
    ISSN 2375-2548 ; 2375-2548
    ISSN (online) 2375-2548
    ISSN 2375-2548
    DOI 10.1126/sciadv.abg6856
    Database MEDical Literature Analysis and Retrieval System OnLINE

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