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  • 1
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    Online Resource
    2092-P: Impact of Insulin Resistance on Response to a Meal by Salience, Executive Control, and Default Mode Resting State Networks in Humans
    American Diabetes Association ; 2019
    In:  Diabetes Vol. 68, No. Supplement_1 ( 2019-06-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 68, No. Supplement_1 ( 2019-06-01)
    Abstract: Functional connectivity (fc) in the Salience Network (SN) is reduced by a meal. We hypothesized that disengagement of the SN may be mirrored by increased fc in Executive Control (ECN) or Default Mode (DMN) networks (representing a switch away from interoceptive neural processing after feeding) and that insulin resistance might impact shifts in postprandial neural processing. Subjects (N=111) oversampled for obesity had body composition, fasting glucose and insulin evaluated and underwent resting-state fMRI before and after a standardized meal. Masks for ECN (Seeley2007) and DMN (Grecius2003) were applied to obtain the fc pre-, post-meal and change (%). Subgroups with low (N=37) and high (N=36) HOMA-IR were created from tertiles. Among all subjects (28±9 y; BMI 30.5±6 kg/m2), ECN fc was reduced by a meal (z=-2.9, P=0.004), but DMN fc did not change (z=-0.02, P=0.98). The low and high HOMA-IR groups had mean BMIs of 26.8 and 34.7±5. Fc response to a meal, adjusted for age, sex and fat mass, did not differ between low and high HOMA groups for ECN (group*time chi2(1)=2.39, PInt=0.12) or SN (chi2(1)=2.52, PInt=0.11); both groups reduced fc. However, for DMN a group*time was found (chi2(1)=9.12, PInt=0.003, adjusted), such that the low HOMA group increased post-meal fc (Fisher z-score 0.36 vs. 0.41, P=0.04), but high HOMA group decreased fc (0.37 vs. 0.31, P=0.03). Change (%) in connectivity was positively correlated among all 3 networks (P & lt;0.002). A significant interaction for DMN vs. ECN (P=0.02) by HOMA group was present. Participants with high HOMA had a blunted correlation between DMN and ECN (coef=0.12, P=0.28) compared to those with low HOMA (coef=0.61, P=0.001). Fc was reduced by a meal in the ECN and not modified in the DMN on average. However, DMN fc increased with feeding in non-insulin resistant individuals as hypothesized, but decreased in those with insulin resistance, suggesting that insulin resistance impacts shifts in neural processing in response to a meal. Disclosure L.E. Sewaybricker: None. S.J. Melhorn: None. M.K. Askren: None. M. Webb: None. V. Tyagi: None. M. De Leon: None. T.J. Grabowski: None. E. Schur: None. Funding American Diabetes Association (1-17-ICTS-085 to E.S.); Sao Paulo Research Foundation (2017/00657-0); National Institutes of Health (DK089036, DK098466); University of Washington Nutrition Obesity Research Center (P30 DK035816); Diabetes Research Center (P30DK017047); Institute of Translational Health Sciences (UL1TR000423)
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db19-2092-P
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2019
    detail.hit.zdb_id: 1501252-9
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  • 2
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    1808-P: Is There Evidence of Gliosis Outside the Mediobasal Hypothalamus in Obese Adults?
    American Diabetes Association ; 2019
    In:  Diabetes Vol. 68, No. Supplement_1 ( 2019-06-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 68, No. Supplement_1 ( 2019-06-01)
    Abstract: Data increasingly support evidence of gliosis in the mediobasal hypothalamus (MBH) in the setting of obesity and insulin resistance. It is if other regions of the brain are similarly affected. We tested if MBH gliosis is related to radiologic evidence of gliosis in selected subcortical, cortical, and hypothalamic regions. We recruited 40 obese adults (aged 25-61 y), with variable glucose tolerance by OGTT (n=24 normal glucose tolerance, n=11 impaired glucose tolerance and n=5 with T2DM). Individuals underwent a multi-echo T2 brain MRI. Two analysts placed regions of interest (ROIs) on the scans and determined the T2 relaxation time as a measure of gliosis. ROIs included the MBH, amygdala, dorsomedial hypothalamus (DMH; area of the paraventricular nucleus), hippocampus, white matter (WM), cortex, caudate, ventral striatum (VS), and putamen. Left and right sides were averaged. High (n=13) and low (n=14) T2 groups were derived from the tertiles with the highest (strongest evidence for gliosis) and lowest T2 relaxation times. The groups were compared by linear regression adjusted for age and sex. Mean BMI in the low T2 group was 35.7 ± 4.1 kg/m2 and high T2 group was 37.1 ± 4.9 kg/m2. The groups did not differ in T2 relaxation time of WM (P=0.29), cortex (P=0.15), caudate (P=0.49), putamen (P=0.79), amygdala (P=0.09), or hippocampus (P=0.44). In the high T2 group, T2 relaxation time was shorter in the VS (adjusted mean 80.9±2.9 vs. 83.1±3.0, P=0.04) and longer in the DMH (adjusted mean 108.9±5.3 vs. 103.7±5.4, P=0.02), compared to the low T2 group. When subjects with T2DM (n=1 in low and n=3 in high T2 group) were excluded, the differences were attenuated (VSP=0.13; DMHP=0.10). The findings reveal preliminary evidence of longer T2 relaxation times in the DMH of obese individuals with signs of MBH gliosis and no evidence for gliosis in cortical or subcortical regions. Further study of gliosis in the DMH and its relation to blood glucose control and autonomic function in humans, particularly in those with T2DM, is warranted. Disclosure J.L. Rosenbaum: None. S.J. Melhorn: None. M. De Leon: None. M. Webb: None. E. Schur: None. Funding American Diabetes Association (1-17-ICTS-085 to E.S.); National Institutes of Health (T32HL007028); University of Washington Institute of Translational Health Sciences (UL1TR002319)
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db19-1808-P
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2019
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  • 3
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    170-OR: Hypothalamic Gliosis Predicts Decline in Insulin Sensitivity over One Year in People with Obesity
    American Diabetes Association ; 2021
    In:  Diabetes Vol. 70, No. Supplement_1 ( 2021-06-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 70, No. Supplement_1 ( 2021-06-01)
    Abstract: Studies demonstrate evidence of gliosis in the mediobasal hypothalamus (MBH) of people with obesity and T2D or impaired glucose tolerance (IGT), but whether MBH gliosis predicts worsening glucose homeostasis is unknown. The study evaluated 38 subjects with obesity (68% female, 76% White). Mean age was 47±11 y and BMI was 35±3.9 kg/m2. MRI, DXA, and 75 g OGTT were performed at baseline and DXA and OGTT repeated at 1y. Mean bilateral T2 relaxation time (ms) in the MBH and 3 control regions was measured as a marker of gliosis. Serial blood samples from OGTT were used to calculate glucose area under the curve (incremental [iAUC] and total [totalAUC] ) and to model insulin sensitivity (OGIS) and beta-cell function (beta-cell glucose sensitivity). Generalized estimating equations tested associations and interactions by region. On average, measures of glucose tolerance (iAUC and totalAUC), OGIS, and beta-cell glucose sensitivity were stable over 1 y. Baseline bilateral mean MBH T2 relaxation time was not associated with changes in glucose tolerance (Δ iAUC β: -5.8 ms, 95% CI -21.0, 9.4, P=0.45; Δ totalAUC β: 1.3 ms, 95% CI -33.5, 36.0, P=0.94, adjusted for sex, age) or change in glucose sensitivity (β: 0.3 ms, 95% CI -1.0, 1.6, P=0.66) nor were interactions present. Change in OGIS over 1y was significantly negatively associated with bilateral mean MBH T2 relaxation time at baseline (β: -0.94 ms, 95% CI -1.7, -0.2, P=0.02, adjusted for sex, age); subjects with longer MBH T2 relaxation times at baseline reduced OGIS over 1 y. A formal interaction by region was not significant (chi2(7)=7.11, Pint=0.42). The relationship within the MBH was attenuated when also adjusted for change in fat mass (β: -0.70 ms 95% CI -1.4, 0.02, P=0.056). Subjects with greater radiologic evidence for MBH gliosis exhibited declines in insulin sensitivity over 1 y which were not fully accounted for by changes in adiposity. These longitudinal findings are consistent with a role for MBH gliosis in T2D pathogenesis in people with obesity. Disclosure J. L. Rosenbaum: None. S. Schoen: None. S. J. Melhorn: None. M. De leon: None. M. Webb: None. K. Utzschneider: None. E. Schur: None. Funding American Diabetes Association (1-17-ICTS-085 to E.S.)
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db21-170-OR
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2021
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  • 4
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    151-OR: Radiologic Evidence that Hypothalamic Tissue Is Abnormal in Adults with Obesity and Type 2 Diabetes or Impaired Glucose Homeostasis
    American Diabetes Association ; 2020
    In:  Diabetes Vol. 69, No. Supplement_1 ( 2020-06-01)
    Details
    In: Diabetes, American Diabetes Association, Vol. 69, No. Supplement_1 ( 2020-06-01)
    Abstract: Gliosis, a cellular response to injury in neural tissue, is linked to diet-induced obesity in rodent models. Growing evidence also implicates reactive gliosis and inflammation of the mediobasal hypothalamus (MBH) as a potential mechanism connecting obesity to insulin resistance. We tested for radiologic evidence of MBH gliosis in humans in relation to impaired glucose homeostasis and type 2 diabetes (T2D), independent of obesity. Adults with obesity and 1) T2D not on insulin (N=17), 2) impaired glucose tolerance (IGT; N=21), or 3) normal glucose tolerance (NGT; N=29) by OGTT underwent magnetic resonance imaging to measure mean bilateral T2 relaxation time (ms) in the MBH and 3 control regions. Longer T2 relaxation time is a marker of gliosis. Groups were matched for race, sex, BMI and % body fat (P=0.99), but age differed (T2D 54 ± 8 y, IGT 46 ± 11 y, NGT 45 ± 12 y; P=0.02). Group differences in T2 relaxation time varied by brain region (interaction: chi2(6) = 65, P & lt;0.0001, adjusted for sex and age). Bonferroni-corrected post-tests confirmed that MBH, but not control region, T2 relaxation times were longer in T2D (180 ± 26 ms) than IGT (160 ± 26 ms, P & lt;0.0001) or NGT (152 ± 17 ms, P & lt;0.0001) groups. Among all 67 subjects, fasting glucose, 2-hr post-glucose, and hemoglobin A1c values were each positively associated with MBH, but not control region, T2 relaxation times (interactions by region all P & lt; 0.0001, MBH all P & lt; 0.0001, control regions all NS). Among the 50 subjects without T2D, interactions remained significant (all P & lt;0.0001), and greater 2-hr post-glucose and hemoglobin A1c were associated with longer MBH T2 relaxation times (β = 0.22 ms, P & lt;0.0001 and β = 14.8 ms, P=0.002, respectively) whereas a trend was present for fasting glucose concentrations (β = 0.38 ms, P=0.06). These data provide novel evidence that the degree of inflammation and gliosis in glucose-regulating areas of the brain is related to impaired glucose homeostasis and T2D in adults with obesity. Disclosure J.L. Rosenbaum: None. L.E. Sewaybricker: None. S. Chandrasekaran: None. M. De Leon: None. M. Webb: None. S.J. Melhorn: None. E. Schur: None. Funding American Diabetes Association (1-17-ICTS-085 to E.S.)
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/db20-151-OR
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2020
    detail.hit.zdb_id: 1501252-9
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  • 5
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    1714-P: Higher Initial Diet Quality Predicts Shorter Weight Loss Period prior to an Involuntary Weight Loss Plateau
    American Diabetes Association ; 2023
    In:  Diabetes Vol. 72, No. Supplement_1 ( 2023-06-20)
    Details
    In: Diabetes, American Diabetes Association, Vol. 72, No. Supplement_1 ( 2023-06-20)
    Abstract: It is currently unknown what factor(s) may promote entry into a weight loss plateau. Given intensive lifestyle interventions (ILI) for weight loss include changes in diet, we evaluated how diet quality impacts characteristics of a weight loss plateau. Daily weights were obtained remotely via electronic scale from 62 adults with obesity (73% female, mean age 42±11 y and BMI 37±5 kg/m2) undergoing a 24-week ILI. Periods (≥14 d) of active weight loss or plateau were identified by threshold regression modeling. Active weight loss was defined as a per day % weight change from baseline equivalent to ≥0.5 lb loss/wk and a weight loss plateau as ±0.25lbs/wk after a period of active weight loss (in which ≥3.5% weight loss was achieved). Three unannounced self-reported ASA24 dietary recalls were obtained at baseline and 3 mo. Diet quality was assessed by the healthy eating index (HEI)-2015. 53% reached a plateau after active weight loss (27% did not achieve & gt;3.5% weight loss, 19% re-gained directly after loss). Weight loss (i.e., plateau depth) was associated with longer time to plateau (β=–10d, P & lt;0.01). Higher baseline diet quality (total HEI) was associated with shorter time to plateau (β=–2.6d, P=0.03), but not overall depth of plateau (β=0.1%, P=0.28). Specifically, shorter time to plateau was related to lower baseline consumption of saturated fats (β=–15d, P=0.01) and greater plateau depth was related to lower baseline consumption of added sugars (β=1.3%, P=0.04). Mean diet quality improved minimally during ILI (ΔHEI 1.9±2.2). Lower baseline HEI correlated with greater improvement in diet quality at 3 mo (β=–0.5, P & lt;0.001, N=46), but ΔHEI did not associate with any plateau characteristics (time: β=1.1d, P=0.15; depth: β=–0.1%, P=0.16, N=25). Higher diet quality upon entry into an ILI predicted a shorter duration of weight loss prior to reaching a plateau, suggesting that individuals with healthy eating patterns may derive less sustained weight loss benefit from participation in an ILI. Disclosure S.J.Melhorn: None. L.E.Sewaybricker: None. H.Gao: None. M.De leon: None. M.Webb: None. M.Lyle: None. S.J.Beatty: None. M.Kratz: Other Relationship; Nourished by Science LLC. E.Schur: None. Funding National Institutes of Health (DK089036, DK1176223, K24HL144917); University of Washington (NORC, DK035816)
    Type of Medium: Online Resource
    ISSN: 0012-1797
    URL: Article
    DOI: 10.2337/db23-1714-P
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2023
    detail.hit.zdb_id: 1501252-9
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  • 6
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    Evidence That Hypothalamic Gliosis Is Related to Impaired Glucose Homeostasis in Adults With Obesity
    American Diabetes Association ; 2022
    In:  Diabetes Care Vol. 45, No. 2 ( 2022-02-01), p. 416-424
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 45, No. 2 ( 2022-02-01), p. 416-424
    Abstract: Preclinical research implicates hypothalamic glial cell responses in the pathogenesis of obesity and type 2 diabetes (T2D). In the current study we sought to translate such findings to humans by testing whether radiologic markers of gliosis in the mediobasal hypothalamus (MBH) were greater in individuals with obesity and impaired glucose homeostasis or T2D. RESEARCH DESIGN AND METHODS Using cross-sectional and prospective cohort study designs, we applied a validated quantitative MRI approach to assess gliosis in 67 adults with obesity and normal glucose tolerance, impaired glucose tolerance (IGT), or T2D. Assessments of glucose homeostasis were conducted via oral glucose tolerance tests (OGTT) and β-cell modeling. RESULTS We found significantly greater T2 relaxation times (a marker of gliosis by MRI), that were independent of adiposity, in the groups with IGT and T2D as compared with the group with normal glucose tolerance. Findings were present in the MBH, but not control regions. Moreover, positive linear associations were present in the MBH but not control regions between T2 relaxation time and glucose area under the curve during an OGTT, fasting glucose concentrations, hemoglobin A1c, and visceral adipose tissue mass, whereas negative linear relationships were present in the MBH for markers of insulin sensitivity and β-cell function. In a prospective cohort study, greater MBH T2 relaxation times predicted declining insulin sensitivity over 1 year. CONCLUSIONS Findings support a role for hypothalamic gliosis in the progression of insulin resistance in obesity and thus T2D pathogenesis in humans.
    Type of Medium: Online Resource
    ISSN: 0149-5992
    URL: Article
    DOI: 10.2337/dc21-1535
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2022
    detail.hit.zdb_id: 1490520-6
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