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1 roperitoneal and epididymal white tissue and IBAT, but skeletal muscle 2-DG uptake under the same con
2  CRFR2 revealed significantly elevated basal IBAT thermogenesis and prolonged adrenergic responsivity
3 pinephrine content of the interscapular BAT (IBAT) and the number of sympathetic ganglion cells proje
4 d receive SS inflow from, interscapular BAT (IBAT) in these separate studies suggesting SNS-SS feedba
5  sympathetically-mediated interscapular BAT (IBAT) thermogenesis.
6 tor-gamma-coactivator1-alpha (PGC-1alpha) in IBAT and increased UCP1protein expression; however, pero
7     Expression of GLUT4 was more abundant in IBAT and retroperitoneal fat from glucose- and fructose-
8 se or fructose, leading to SNS activation in IBAT and retroperitoneal fat and enhanced GLUT4 expressi
9  essential role in mediating the increase in IBAT thermogenesis induced by activation of central mela
10                             The increases in IBAT SNA and in O(2) consumption were reversed by inhibi
11 roup of rats, the neural circuit involved in IBAT control, including the location of sympathetic preg
12  expression, or decreased UCP1 mRNA level in IBAT.
13             In addition, UCP1 mRNA levels in IBAT did not change with age.
14 ke in IBAT of the KE group was twice that in IBAT of the Ctrl group.
15  by contrast, decreased [(3)H]NE turnover in IBAT, but increased it in epididymal, though not retrope
16         [(18)F]-Fluorodeoxyglucose uptake in IBAT of the KE group was twice that in IBAT of the Ctrl
17 NH2; 0.024nmol) both significantly increased IBAT temperature (T(IBAT)) and pretreatment with the MC4
18            CL316,243 significantly increased IBAT temperature, afferent nerve activity, and c-Fos-IR
19 stalk by injecting both PRV152 and H129 into IBAT of Siberian hamsters.
20  the central nervous system (CNS) control of IBAT thermogenesis.
21                Pharmacological inhibition of IBAT with GSK2330672 may reduce BA levels in the systemi
22 lly linked to the sympathetic innervation of IBAT.
23 sis and prolonged adrenergic responsivity of IBAT in older mice.
24 y c-Fos immunoreactivity (IR), we prelabeled IBAT DRG innervating neurons by injecting the retrograde
25 of MTII (1 nmol) significantly increased rat IBAT SNA (+741% of control).
26 R antagonist alone significantly decreased T(IBAT) up to 3h post injection.
27 locked the MC4-R agonist-induced increased T(IBAT) in conscious, freely-moving Siberian hamsters.
28 icle-treated hamsters initially maintained T(IBAT), but the ability of the former waned after 2 h bei
29 sters and, when they were adults, measured T(IBAT) during acute cold exposure.
30  reported to be involved in the control of T(IBAT).
31 ical increases in the duration and peak of T(IBAT).
32 nability of MSG-treated animals to sustain T(IBAT) in the cold is not due to any obvious MSG-induced
33  significantly increased IBAT temperature (T(IBAT)) and pretreatment with the MC4R antagonist, HS024
34 , although, interscapular BAT temperature (T(IBAT)) has not been measured.
35 al design of future development phase of the IBAT inhibitor drug.
36 nover in interscapular brown adipose tissue (IBAT) and retroperitoneal fat increased in response to g
37 evels in interscapular brown adipose tissue (IBAT) from F344 x BN rats ages 3, 12, 18, 24, and 30 mon
38 ivity of interscapular brown adipose tissue (IBAT) in response to physiologic stimuli, such as cold e
39 lyses of interscapular brown adipose tissue (IBAT) thermogenesis by thermal signature analysis and th
40 n affect interscapular brown adipose tissue (IBAT) thermogenesis via its sympathetic nervous system (
41 scle and interscapular brown adipose tissue (IBAT) was investigated.
42 s, while interscapular brown adipose tissue (IBAT) weight doubled.
43 s in the interscapular brown adipose tissue (IBAT).
44 eased sympathetic nervous system activity to IBAT.
45 s of central sympathetic outflow circuits to IBAT, but appears to be extrinsic to the tissue neverthe
46 th components of the CNS outflow circuits to IBAT, with the latter implicated in BAT thermogenesis th
47 ons of MC4-R mRNA and SNS outflow neurons to IBAT that has not been previously reported to be involve
48  co-localization with SNS outflow neurons to IBAT, the subzona incerta (subZI) to test whether IBAT t
49 groups related to the sympathetic outflow to IBAT also were identified.
50 e for the increase in sympathetic outflow to IBAT during cold-evoked thermogenesis.
51 d-evoked increases in sympathetic outflow to IBAT, the present study compared central nervous system
52 a on the sympathetic nerve activity (SNA) to IBAT evoked by lateral ventricular injection of the mela
53             The ileal bile acid transporter (IBAT) protein expressed in the distal ileum plays a key
54 d importer, the ileal bile acid transporter (IBAT), as well as for CBATP.
55 ibitor of human ileal bile acid transporter (IBAT), in patients with primary biliary cholangitis with
56                   The results show that when IBAT mediates uptake of [3H]taurocholate to a level 20-f
57  the subzona incerta (subZI) to test whether IBAT thermogenesis could be increased or decreased.
58 was detected in COS cells cotransfected with IBAT and a chimeric molecule having the carboxyl-termina
59  acid efflux in COS cells cotransfected with IBAT and CEA, efflux of [3H]taurocholate was detected in

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