Duodenal lipid sensing increases BAT temperature.

<p>(A) BAT temperature 10 min prior to and 120 min following a 30 min intraduodenal infusion of 5 ml saline or IL 10%. (B) BAT temperature expressed as a % of baseline at 30, 60, 90 and 120 min following the beginning of a 30 min intraduodenal infusion of 5 ml saline or IL 10%. All data are means ± SEM, n = 7. *: p<0.05.</p

CCKA receptor blockade blunts duodenal lipid-induced BAT thermogenesis.

<p>BAT temperature expressed as a % of baseline at 30, 60, 90 and 120 min following the beginning of a 30 min intraduodenal infusion of 5 ml saline or IL 10% and preceded by an intraperitoneal injection of DVZ or vehicle. All data are means ± SEM, n = 6–7. Means that share a common letter do no significantly differ from one another.</p

NTS NMDA receptor blockade blunts duodenal lipid-induced BAT thermogenesis.

<p>BAT temperature expressed as a % of baseline at 30, 60, 90 and 120 min following the beginning of a 30 min intraduodenal infusion of 5 ml saline or IL 10% and preceded with an bilateral NTS injection of MK801 or vehicle. All data are means ± SEM, n = 7. Means that share a common letter do no significantly differ from one another.</p

Impaired anorectic effect of cmNTs L-leucine in HF-fed and diet-induced obese mice.

<p>24h food intake, meal size, meal number and first meal size following a cmNTS injection of aCSF or L-leucine 105pmol/side in mice fed a LF- or HF-diet for 6 months (a, b), 1050pmol/side in mice fed a LF- or HF-diet for 6 months (c,d), or 105pmol/side in mice fed a LF- or HF-diet for 2 weeks (e,f). N = 5–6, *: P<0.05. **: P<0.01</p

Impaired activity of the cmNTS p70 S6 kinase 1 pathway in HF-fed mice.

<p>p70 S6 kinase 1 Thr389 phosphorylation in the cmNTS of (a) chow-fed mice or HF-fed mice (n = 5–6). Distribution of phosphorylated S6 ribosomal protein in the cmNTS of 6h-fasted (b) chow-fed mice or (c) HF diet-fed mice. Colocalization (right, orange) or phosphorylated ribosomal protein S6 (p-rpS6, middle, red) and POMC (d), TH (e) or DBH (f) (left, green) in the cmNTS of 6h-fasted HF-fed mice. Scale bar: 50 μm. First meal size, first meal latency and food intake in LF-fed (g, n = 5) or HF-fed (h, n = 5) pre-sated mice following a cmNTS injected of rapamycin or vehicle. *: P<0.05.</p

Impaired cmNTS metabolic integration in DIO mice.

<p>(a) 30 min food intake in chow-fed or HF-fed mice following ip injection of different doses of CCK. 30 min food intake following the combination of an anorectic dose of L-leucine injected into the cmNTS together with a subthreshold ip CCK dose in (b) chow-fed mice (leucine: 105pmol/side, CCK: 1 <b>μ</b>g/kg) or (c) high-fat fed (leucine: 1.05nmol/side, CCK: 2 <b>μ</b>g/kg) mice. n = 5–6, *: P<0.05, **: P<0.01</p

cmNTS L-leucine reduces food intake and body weight gain in chow fed mice.

<p>(a) cmNTS distribution of fluorescent-labeled L-leucine following a cmNTS targeted injection with inverted colors. ap: area postrema, cc: central canal, DMX: vagus nerve X. (b) Food intake, (c) 24h body weight change, (d) first meal size, (e) first meal latency, (f) meal size and (g) meal number 6h fasted mice following a cmNTS injection of L-leucine or vehicle. n = 10–12, *: P<0.05, **: P<0.01</p

Locomotor Activity And Metabolic Functions In Leptin Treated MKR Mice.

<p>Two week third intracerebroventricular leptin treatment (black bars) reduced light and dark phase locomotor activity (A,B), respiratory quotient (RER, C,D) and increased both light and dark phase oxygen consumption in male MKR mice relative to artificial cerebrospinal fluid (ACSF) vehicle treated controls (open bars) (E,F). All data presented as means ± SEM, N = 6/group. * p<0.05.</p

Body Weights (A) And Fat Content (B), Before And After 14 Days Of ICV Leptin Treatment Compared With ACSF And Pair-Fed Control Mice.

<p>All data presented as means ± SEM, N = 6–7/group. * p<0.05. Different superscript letters indicate significant differences at p<0.05.</p

Hyperinsulinemic-euglycemic clamps.

<p>Third intracerebroventricular leptin treatment (black bars) significantly improved hepatic insulin sensitivity and glucose disposal during hyperinsulinemic-euglycemic clamps in male MKR mice relative to artificial cerebrospinal fluid (ACSF) vehicle treated controls (open bars) and pair fed, ACSF treated male MKR mice (hatched bars). A. Glucose infusion rate (GIR) during the clamp, B. peripheral glucose disappearance rate (Rd), hepatic glucose production (GP) under basal conditions (C) or hyperinsulinemia (D). All data presented as means ± SEM. N = 5–6/group. Different superscript letters indicate significant differences at p<0.05.</p