GLORIA

GEOMAR Library Ocean Research Information Access

X

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
Material
Publisher
Person/Organisation
Language
Years
FID
Subjects(RVK)
  • 1
    Online Resource
    Online Resource
    Optimization of Metformin in the GRADE Cohort: Effect on Glycemia and Body Weight
    American Diabetes Association ; 2020
    In:  Diabetes Care Vol. 43, No. 5 ( 2020-05-01), p. 940-947
    Details
    In: Diabetes Care, American Diabetes Association, Vol. 43, No. 5 ( 2020-05-01), p. 940-947
    Abstract: We evaluated the effect of optimizing metformin dosing on glycemia and body weight in type 2 diabetes. RESEARCH DESIGN AND METHODS This was a prespecified analysis of 6,823 participants in the Glycemia Reduction Approaches in Diabetes: A Comparative Effectiveness Study (GRADE) taking metformin as the sole glucose-lowering drug who completed a 4- to 14-week (mean ± SD 7.9 ± 2.4) run-in in which metformin was adjusted to 2,000 mg/day or a maximally tolerated lower dose. Participants had type 2 diabetes for & lt;10 years and an HbA1c ≥6.8% (51 mmol/mol) while taking ≥500 mg of metformin/day. Participants also received diet and exercise counseling. The primary outcome was the change in HbA1c during run-in. RESULTS Adjusted for duration of run-in, the mean ± SD change in HbA1c was −0.65 ± 0.02% (−7.1 ± 0.2 mmol/mol) when the dose was increased by ≥1,000 mg/day, −0.48 ± 0.02% (−5.2 ± 0.2 mmol/mol) when the dose was unchanged, and −0.23 ± 0.07% (−2.5 ± 0.8 mmol/mol) when the dose was decreased (n = 2,169, 3,548, and 192, respectively). Higher HbA1c at entry predicted greater reduction in HbA1c (P & lt; 0.001) in univariate and multivariate analyses. Weight loss adjusted for duration of run-in averaged 0.91 ± 0.05 kg in participants who increased metformin by ≥1,000 mg/day (n = 1,894). CONCLUSIONS Optimizing metformin to 2,000 mg/day or a maximally tolerated lower dose combined with emphasis on medication adherence and lifestyle can improve glycemia in type 2 diabetes and HbA1c values ≥6.8% (51 mmol/mol). These findings may help guide efforts to optimize metformin therapy among persons with type 2 diabetes and suboptimal glycemic control.
    Type of Medium: Online Resource
    ISSN: 0149-5992 , 1935-5548
    URL: Article
    DOI: 10.2337/dc19-1769
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2020
    detail.hit.zdb_id: 1490520-6
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 2
    Online Resource
    Online Resource
    Sympathetic and Cardiorenal Actions of Leptin
    Ovid Technologies (Wolters Kluwer Health) ; 1997
    In:  Hypertension Vol. 30, No. 3 ( 1997-09), p. 619-623
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 30, No. 3 ( 1997-09), p. 619-623
    Abstract: Abstract Body weight is tightly regulated physiologically. The recent discovery of the peptide hormone leptin has permitted more detailed evaluation of the mechanisms responsible for control of body fat. Leptin is almost exclusively produced by adipose tissue and acts in the CNS through a specific receptor and multiple neuropeptide pathways to decrease appetite and increase energy expenditure. Leptin thus functions as the afferent component of a negative feedback mechanism to control adipose tissue mass. Increasing evidence suggests that leptin may have wider actions influencing autonomic, cardiovascular, and endocrine function. Intravenous leptin increases norepinephrine turnover and sympathetic nerve activity to thermogenic brown adipose tissue. Studies from our laboratory suggest that leptin also increases sympathetic nerve activity to kidney, hindlimb, and adrenal gland. However, systemic administration of leptin does not acutely increase arterial pressure or heart rate in anesthetized animals. Thus, longer-term exposure to hyperleptinemia may be necessary for full expression of the expected pressor effect of renal sympathoexcitation. Alternatively, leptin may have additional cardiovascular actions to oppose sympathetically mediated vasoconstriction. Leptin in high doses increases renal sodium and water excretion, apparently through a direct tubular action. In addition, leptin appears to increase systemic insulin sensitivity, even in the absence of weight loss. Although we are at an early stage of understanding, we speculate that abnormalities in the actions of leptin may have implications for the sympathetic, cardiovascular, and renal changes associated with obesity.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.30.3.619
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1997
    detail.hit.zdb_id: 2094210-2
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 3
    Online Resource
    Online Resource
    Interactions Between the Melanocortin System and Leptin in Control of Sympathetic Nerve Traffic
    Ovid Technologies (Wolters Kluwer Health) ; 1999
    In:  Hypertension Vol. 33, No. 1 ( 1999-01), p. 542-547
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 33, No. 1 ( 1999-01), p. 542-547
    Abstract: Abstract —Leptin plays an important role in regulation of body weight through regulation of food intake and sympathetically mediated thermogenesis. The hypothalamic melanocortin system, via activation of the melanocortin-4 receptor (MC4-R), decreases appetite and weight, but its effects on sympathetic nerve activity (SNA) are unknown. In addition, it is not known whether sympathoactivation to leptin is mediated by the melanocortin system. We tested the interactions between these systems in regulation of brown adipose tissue (BAT) and renal and lumbar SNA in anesthetized Sprague-Dawley rats. Intracerebroventricular administration of the MC4-R agonist MT-II (200 to 600 pmol) produced a dose-dependent sympathoexcitation affecting BAT and renal and lumbar beds. This response was completely blocked by the MC4-R antagonist SHU9119 (30 pmol ICV). Administration of leptin (1000 μg/kg IV) slowly increased BAT SNA (baseline, 41±6 spikes/s; 6 hours, 196±28 spikes/s; P =0.001) and renal SNA (baseline, 116±16 spikes/s; 6 hours, 169±26 spikes/s; P =0.014). Intracerebroventricular administration of SHU9119 did not inhibit leptin-induced BAT sympathoexcitation (baseline, 35±7 spikes/s; 6 hours, 158±34 spikes/s; P =0.71 versus leptin alone). However, renal sympathoexcitation to leptin was completely blocked by SHU9119 (baseline, 142±17 spikes/s; 6 hours, 146±25 spikes/s; P =0.007 versus leptin alone). This study demonstrates that the hypothalamic melanocortin system can act to increase sympathetic nerve traffic to thermogenic BAT and other tissues. Our data also suggest that leptin increases renal SNA through activation of hypothalamic melanocortin receptors. In contrast, sympathoactivation to thermogenic BAT by leptin appears to be independent of the melanocortin system.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.33.1.542
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1999
    detail.hit.zdb_id: 2094210-2
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 4
    Online Resource
    Online Resource
    Plasma leptin in diabetic and insulin-treated diabetic and normal rats
    Elsevier BV ; 1998
    In:  Metabolism Vol. 47, No. 5 ( 1998-5), p. 584-591
    Details
    In: Metabolism, Elsevier BV, Vol. 47, No. 5 ( 1998-5), p. 584-591
    Type of Medium: Online Resource
    ISSN: 0026-0495
    URL: Article
    DOI: 10.1016/S0026-0495(98)90244-X
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1998
    detail.hit.zdb_id: 2049062-8
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 5
    Online Resource
    Online Resource
    Obesity impairs vascular relaxation in human subjects: hyperglycemia exaggerates adrenergic vasoconstriction
    Elsevier BV ; 2007
    In:  Journal of Diabetes and its Complications Vol. 21, No. 3 ( 2007-5), p. 149-157
    Details
    In: Journal of Diabetes and its Complications, Elsevier BV, Vol. 21, No. 3 ( 2007-5), p. 149-157
    Type of Medium: Online Resource
    ISSN: 1056-8727
    URL: Article
    DOI: 10.1016/j.jdiacomp.2005.12.003
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2007
    detail.hit.zdb_id: 2006763-X
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 6
    Online Resource
    Online Resource
    Leptin Potentiates Thermogenic Sympathetic Responses to Hypothermia
    American Diabetes Association ; 2002
    In:  Diabetes Vol. 51, No. 8 ( 2002-08-01), p. 2434-2440
    Details
    In: Diabetes, American Diabetes Association, Vol. 51, No. 8 ( 2002-08-01), p. 2434-2440
    Abstract: Leptin contributes to the regulation of thermogenesis. In rodents, sympathetic nerve activity efferent to interscapular brown adipose tissue (IBAT-SNA) is involved. On the basis of the hypotheses that 1) leptin acutely potentiates hypothermia-induced increases in IBAT-SNA; 2) this action of leptin is specific to IBAT-SNA, i.e., it does not occur with renal sympathetic nerve activity (R-SNA); and 3) this effect of leptin depends on intact and functional leptin receptors, we measured IBAT-SNA and R-SNA in anesthetized lean and diet-induced obese Sprague-Dawley and in obese Zucker rats, randomly assigned to low-dose leptin or vehicle. Before the start of leptin or vehicle and 5 min, 90 min, and 180 min after, hypothermia (30° C) was induced. Compared with vehicle, leptin did not significantly alter baseline R-SNA or IBAT-SNA. In lean Sprague-Dawley rats, hypothermia-induced increases in IBAT-SNA were significantly augmented by leptin but not by vehicle. In obese Sprague-Dawley rats, leptin did not potentiate hypothermia-induced increases in IBAT-SNA. In Zucker rats, IBAT-SNA did not increase with hypothermia and leptin was not able to induce sympathoactivation with cooling. Changes in R-SNA during hypothermia were not significantly modified by leptin in either group. Thus, low-dose leptin, although not altering baseline SNA, acutely enhances hypothermia-induced sympathetic outflow to IBAT in lean rats. This effect is specific for thermogenic SNA because leptin does not significantly alter the response of R-SNA to hypothermia. The effect depends on intact and functional leptin receptors because it occurs neither in rats with a leptin receptor defect nor in rats with acquired leptin resistance.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/diabetes.51.8.2434
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2002
    detail.hit.zdb_id: 1501252-9
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 7
    Online Resource
    Online Resource
    Effect of Acute and Antecedent Hypoglycemia on Sympathetic Neural Activity and Catecholamine Responsiveness in Normal Rats
    American Diabetes Association ; 2001
    In:  Diabetes Vol. 50, No. 5 ( 2001-05-01), p. 1119-1125
    Details
    In: Diabetes, American Diabetes Association, Vol. 50, No. 5 ( 2001-05-01), p. 1119-1125
    Abstract: Adrenergic responsiveness to acute hypoglycemia is impaired after prior episodes of hypoglycemia. Although circulating epinephrine responses are blunted, associated alterations in adrenal sympathetic nerve activity (SNA) have not been reported. We examined adrenal nerve traffic in normal conscious rats exposed to acute insulin-induced hypoglycemia compared with insulin with (clamped) euglycemia. We also examined adrenal SNA and catecholamine responses to insulin-induced hypoglycemia in normal conscious rats after two antecedent episodes of hypoglycemia (days −2 and −1) compared with prior episodes of sham treatment. Acute insulin-induced hypoglycemia increased adrenal sympathetic nerve traffic compared with insulin administration with clamped euglycemia (165 ± 12 vs. 118 ± 21 spikes/s [P & lt; 0.05]; or to 138 ± 8 vs. 114 ± 10% of baseline [P & lt; 0.05]). In additional experiments, 2 days of antecedent hypoglycemia (days –2 and –1) compared with sham treatment significantly enhanced baseline adrenal SNA measured immediately before subsequent acute hypoglycemia on day 0 (180 ± 11 vs. 130 ± 12 spikes/s, respectively; P & lt; 0.005) and during subsequent acute hypoglycemia (229 ± 17 vs. 171 ± 16 spikes/s; P & lt; 0.05). However, antecedent hypoglycemia resulted in a nonsignificant reduction in hypoglycemic responsiveness of adrenal SNA when expressed as percent increase over baseline (127 ± 5% vs. 140 ± 14% of baseline). Antecedent hypoglycemia, compared with sham treatment, resulted in diminished epinephrine responsiveness to subsequent hypoglycemia. Norepinephrine responses to hypoglycemia were not significantly altered by antecedent hypoglycemia. In summary, prior hypoglycemia in normal rats increased adrenal sympathetic tone, but impaired epinephrine responsiveness to acute hypoglycemia. Hence, these data raise the intriguing possibility that increased sympathetic tone resulting from antecedent hypoglycemia downregulates subsequent epinephrine responsiveness to hypoglycemia. Alternatively, it is possible that the decrease in epinephrine responsiveness after antecedent hypoglycemia could be the result of reduced adrenal sympathetic nerve responsiveness.
    Type of Medium: Online Resource
    ISSN: 0012-1797 , 1939-327X
    URL: Article
    DOI: 10.2337/diabetes.50.5.1119
    Language: English
    Publisher: American Diabetes Association
    Publication Date: 2001
    detail.hit.zdb_id: 1501252-9
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 8
    Online Resource
    Online Resource
    CARDIOVASCULAR CONSEQUENCES OF OBESITY: ROLE OF LEPTIN
    Wiley ; 1998
    In:  Clinical and Experimental Pharmacology and Physiology Vol. 25, No. 1 ( 1998-01), p. 65-69
    Details
    In: Clinical and Experimental Pharmacology and Physiology, Wiley, Vol. 25, No. 1 ( 1998-01), p. 65-69
    Type of Medium: Online Resource
    ISSN: 0305-1870 , 1440-1681
    URL: Issue
    URL: Article
    DOI: 10.1111/cep.1998.25.issue-1
    DOI: 10.1111/j.1440-1681.1998.tb02147.x
    Language: English
    Publisher: Wiley
    Publication Date: 1998
    detail.hit.zdb_id: 2020033-X
    SSG: 15,3
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 9
    Online Resource
    Online Resource
    Adiponectin and C-reactive protein in obesity, type 2 diabetes, and monodrug therapy
    Elsevier BV ; 2004
    In:  Metabolism Vol. 53, No. 11 ( 2004-11), p. 1454-1461
    Details
    In: Metabolism, Elsevier BV, Vol. 53, No. 11 ( 2004-11), p. 1454-1461
    Type of Medium: Online Resource
    ISSN: 0026-0495
    URL: Article
    DOI: 10.1016/j.metabol.2004.06.013
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2004
    detail.hit.zdb_id: 2049062-8
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
  • 10
    Online Resource
    Online Resource
    Role of Corticotrophin-Releasing Factor in Effects of Leptin on Sympathetic Nerve Activity and Arterial Pressure
    Ovid Technologies (Wolters Kluwer Health) ; 2001
    In:  Hypertension Vol. 38, No. 3 ( 2001-09), p. 384-388
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 38, No. 3 ( 2001-09), p. 384-388
    Abstract: Leptin and corticotrophin-releasing factor increase sympathetic nervous activity to interscapular brown adipose tissue, kidneys, and adrenal glands. Leptin is known to increase hypothalamic corticotrophin-releasing factor. In this study, we tested the hypothesis that leptin-dependent increases in sympathetic nervous activity are mediated through increases in central nervous system corticotrophin-releasing factor activity. We examined the effects of intracerebroventricular administration of corticotrophin-releasing factor and intravenous leptin on sympathetic nervous activity to interscapular brown adipose tissue through multifiber neurography in anesthetized Sprague-Dawley rats pretreated with intracerebroventricular α-helical corticotrophin-releasing factor 9–41 (corticotrophin-releasing factor receptor antagonist) or vehicle. Centrally administered corticotrophin-releasing factor substantially increased interscapular brown adipose tissue sympathetic nervous activity. The responses to corticotrophin-releasing factor were substantially attenuated in animals pretreated with α-helical corticotrophin-releasing factor 9–41 . Leptin-dependent increases in interscapular brown adipose tissue sympathetic nervous activity were significantly inhibited by pretreatment with α-helical corticotrophin-releasing factor 9–41 . Interestingly, leptin also significantly increased arterial pressure over 6 hours, but this pressor action was not attenuated by the corticotrophin-releasing factor receptor antagonist. These results suggest that corticotrophin-releasing factor may mediate the sympathoexcitatory effect of leptin on thermogenic tissue without altering its cardiovascular actions.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/01.HYP.38.3.384
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2001
    detail.hit.zdb_id: 2094210-2
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
    Online Resource
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...