LPS inhibits fasted plasma ghrelin levels in rats: role of IL-1 and PGs and functional implications

2006 ◽  
Vol 291 (4) ◽  
pp. G611-G620 ◽  
Author(s):  
Lixin Wang ◽  
Nicole R. Basa ◽  
Almaas Shaikh ◽  
Andrew Luckey ◽  
David Heber ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Gastric Emptying ◽  
Food Intake ◽  
Intravenous Injection ◽  
Plasma Levels ◽  
Inhibitory Action ◽  
Functional Implications ◽  
Urocortin 1 ◽  
Fasted Rats

LPS injected intraperitoneally decreases fasted plasma levels of ghrelin at 3 h postinjection in rats. We characterized the inhibitory action of LPS on plasma ghrelin and whether exogenous ghrelin restores LPS-induced suppression of food intake and gastric emptying in fasted rats. Plasma ghrelin and insulin and blood glucose were measured after intraperitoneal injection of LPS, intravenous injection of IL-1β and urocortin 1, and in response to LPS under conditions of blockade of IL-1 or CRF receptors by subcutaneous injection of IL-1 receptor antagonist (IL-1Ra) or astressin B, respectively, and prostaglandin (PG) synthesis by intraperitoneal indomethacin. Food intake and gastric emptying were measured after intravenous injection of ghrelin at 5 h postintraperitoneal LPS injection. LPS inhibited the elevated fasted plasma ghrelin levels by 47.6 ± 4.9%, 58.9 ± 3.3%, 74.4 ± 2.7%, and 48.9 ± 8.7% at 2, 3, 5, and 7 h postinjection, respectively, and values returned to preinjection levels at 24 h. Insulin levels were negatively correlated to those of ghrelin, whereas there was no significant correlation between glucose and ghrelin. IL-1Ra and indomethacin prevented the first 3-h decline in ghrelin levels induced by LPS, whereas astressin B did not. IL-1β inhibited plasma ghrelin levels, whereas urocortin 1 had no influence. Ghrelin injected intravenously prevented an LPS-induced 87% reduction of gastric emptying and 61% reduction of food intake. These data showed that IL-1 and PG pathways are part of the early mechanisms by which LPS suppresses fasted plasma ghrelin and that exogenous ghrelin can normalize LPS-induced-altered digestive functions.

Abdominal surgery-induced delayed gastric emptying in rats: role of CRF and sensory neurons

1992 ◽  
Vol 262 (4) ◽  
pp. G616-G620 ◽  
Author(s):  
E. Barquist ◽  
M. Zinner ◽  
J. Rivier ◽  
Y. Tache
Keyword(s):  
Gastric Emptying ◽  
Abdominal Surgery ◽  
Intravenous Injection ◽  
Delayed Gastric Emptying ◽  
Phenol Red ◽  
Afferent Neurons ◽  
Afferent Pathways ◽  
Enflurane Anesthesia ◽  
Fasted Rats

The role of peripheral corticotropin-releasing factor (CRF) and afferent pathways in mediating abdominal surgery-induced delayed gastric emptying was investigated using an intravenous injection of the competitive CRF antagonist alpha-helical CRF9-41 and capsaicin pretreatment in adult fasted rats. Gastric emptying of a non-caloric solution was measured by the phenol red method. Intravenous CRF (0.13 nmol) inhibited by 65% gastric emptying. CRF effect was completely reversed by simultaneous intravenous injection of alpha-helical CRF9-41 (13 nmol). Abdominal surgery under enflurane anesthesia inhibited gastric emptying by 60% measured 3 h postoperatively. Enflurane anesthesia alone had no effect on gastric emptying 3 h after exposure. Abdominal surgery-induced delay of gastric emptying was reversed by 46, 60, and 100% by capsaicin pretreatment (125 mg/kg, -3 wk), intravenous injection of alpha-helical CRF9-41 (13 nmol), and combined pretreatments with capsaicin and CRF antagonist, respectively. Capsaicin and alpha-helical CRF9-41 given alone or in combination did not influence gastric emptying. These results indicate that peripheral CRF receptors along with capsaicin-sensitive afferent neurons contribute to somatovisceral stress (abdominal surgery)-induced delayed gastric emptying.

Peripheral urocortin inhibits gastric emptying and food intake in mice: differential role of CRF receptor 2

2001 ◽  
Vol 281 (5) ◽  
pp. R1401-R1410 ◽  
Author(s):  
Lixin Wang ◽  
Vicente Martínez ◽  
Jean E. Rivier ◽  
Yvette Taché
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Corticotropin Releasing Factor ◽  
Delay Gastric Emptying ◽  
Urocortin 1 ◽  
Urocortin 3 ◽  
Cumulative Food Intake

Intraperitoneal urocortin inhibits gastric emptying and food intake in mice. We investigated corticotropin-releasing factor receptor (CRF-R) subtypes involved in intraperitoneal urocortin actions using selective CRF-R antagonists. Gastric emptying was measured 2 h after a chow meal, and food intake was measured hourly after an 18-h fast in mice. Urocortin (3 μg/kg ip) inhibited gastric emptying by 88%. The CRF-R1/CRF-R2 antagonist astressin B (30 μg/kg ip) and the selective CRF-R2 antagonist antisauvagine-30 (100 μg/kg ip) completely antagonized urocortin action, whereas the selective CRF-R1 antagonist CP-154,526 (10 mg/kg ip) had no effect. Urocortin (1–10 μg/kg ip) dose dependently decreased the 2-h cumulative food intake by 30–62%. Urocortin (3 μg/kg)-induced hypophagia was completely antagonized by astressin B (30 μg/kg ip) and partially (35 and 31%) by antisauvagine-30 (100 or 200 μg/kg ip). The CRF-R1 antagonists CP-154,526 or DMP904 (10 mg/kg ip) had no effect. Capsaicin did not alter urocortin-inhibitory actions while blocking the satiety effect of intraperitoneal CCK. These data indicate that intraperitoneal urocortin-induced decrease in feeding is only partly mediated by CRF-R2, whereas urocortin action to delay gastric emptying of a meal involves primarily CRF-R2.

scholarly journals Gastric Sensory and Motor Functions and Energy Intake in Health and Obesity—Therapeutic Implications

Nutrients ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 1158
Author(s):  
Lizeth Cifuentes ◽  
Michael Camilleri ◽  
Andres Acosta
Keyword(s):  
Energy Consumption ◽  
Gastric Emptying ◽  
Food Intake ◽  
Gastric Volume ◽  
Obesity Management ◽  
Bariatric Endoscopy ◽  
Motor Functions ◽  
Therapeutic Implications ◽  
Intestinal Functions

Sensory and motor functions of the stomach, including gastric emptying and accommodation, have significant effects on energy consumption and appetite. Obesity is characterized by energy imbalance; altered gastric functions, such as rapid gastric emptying and large fasting gastric volume in obesity, may result in increased food intake prior to reaching usual fullness and increased appetite. Thus, many different interventions for obesity, including different diets, anti-obesity medications, bariatric endoscopy, and surgery, alter gastric functions and gastrointestinal motility. In this review, we focus on the role of the gastric and intestinal functions in food intake, pathophysiology of obesity, and obesity management.

Control of fructose 2,6-diphosphate in muscle of exercising fasted rats

1992 ◽  
Vol 262 (6) ◽  
pp. E919-E924 ◽  
Author(s):  
W. W. Winder ◽  
C. Duan
Keyword(s):  
Blood Glucose ◽  
Lactate Production ◽  
Quadriceps Muscle ◽  
Active Muscle ◽  
Lower Blood Glucose ◽  
Lower Blood ◽  
Exercise Induced ◽  
Grade One ◽  
Fasted Rats

This study examined the role of epinephrine in controlling intramuscular signals that may accelerate lactate production in less active muscles during exercise. Sham-operated (sham) or adrenodemedullated (ADM) rats were fasted 24 h and then were killed at rest or after running for 15 or 30 min on a treadmill (21 m/min, 15% grade). One-half of the ADM rats were infused with epinephrine (6 micrograms/h) intravenously (jugular catheter) during exercise. ADM rats exhibited lower blood glucose, blood lactate, white quadriceps muscle content of lactate, glucose 6-phosphate, fructose 6-phosphate, and adenosine 3',5'-cyclic monophosphate (cAMP) during exercise than did sham rats or epinephrine-infused ADM rats. The white quadriceps muscle contents of fructose 2,6-diphosphate (F-2,6-P2) and glucose 1,6-diphosphate (G-1,6-P2) (allosteric activators of glycolysis) were at least two times as high in sham rats and in epinephrine-infused rats as in ADM rats during exercise. We conclude that the exercise-induced rise in epinephrine is responsible for the acceleration of glycolysis in less active muscle during exercise. This effect is likely mediated by epinephrine-induced increases in cAMP, F-2,6-P2, and G-1,6-P2.

scholarly journals Electroacupuncture at ST36 Improve the Gastric Motility by Affecting Neurotransmitters in the Enteric Nervous System in Type 2 Diabetic Rats

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Xu Han ◽  
Xiaoyan Chen ◽  
Xuan Wang ◽  
Meirong Gong ◽  
Mengjiang Lu ◽  
...  
Keyword(s):  
Nervous System ◽  
Body Weight ◽  
Blood Glucose ◽  
Gastric Emptying ◽  
Food Intake ◽  
Enteric Nervous System ◽  
The Body ◽  
Antral Motility ◽  
Excitatory Neurotransmitters

Electroacupuncture (EA) can effectively relieve hyperglycemia and gastric emptying disorders in diabetic gastroparesis (DGP). However, the effect of EA on type 2 diabetes mellitus (T2DM) gastroparesis and its mechanism in the enteric nervous system (ENS) are rarely studied. We investigated the therapeutic effect of EA at ST36 and its effect on the main inhibitory and excitatory neurotransmitters in the ENS in DGP rats. Male Sprague-Dawley (SD) rats were fed a high-fat diet for 2 weeks and injected with streptozotocin (STZ) at 35 mg/kg to induce T2DM. T2DM rats were divided into the diabetic mellitus (DM) group and the EA group. The control (CON) group comprised normal rats without any intervention. EA treatment was started 6 weeks after the induction of DM and continued for 5 weeks. The body weight and food intake of the rats were recorded every week. Blood glucose, insulin, glucose tolerance, gastric emptying, and antral motility were measured after treatment. The expression of protein gene product 9.5 (PGP9.5), neuronal nitric oxide synthase (nNOS), and choline acetyltransferase (ChAT) in gastric antrum were quantified by western blotting and quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR). The T2DM gastroparesis model was successfully established. EA treatment reduced the body weight, food intake, and blood glucose; improved glucose intolerance and insulin resistance; increased the gastric emptying rate, the mean antral pressure, and the amplitude of antral motility; and decreased the frequency of antral motility compared with those in the DM group. EA treatment increased the expression level of nNOS, ChAT, and PGP9.5 proteins, and nNOS and ChAT mRNA. The results suggested that EA at ST36 could ameliorate DGP, partly restore the damage to general neurons, and increase nNOS and ChAT in the gastric antrum. EA improved DGP partly via reducing the loss of inhibitory and excitatory neurotransmitters in the ENS.

scholarly journals Intestinal serine protease inhibition increases FGF21 and improves metabolism in obese mice

2019 ◽  
Vol 316 (5) ◽  
pp. G653-G667 ◽  
Author(s):  
Kamal Albarazanji ◽  
Matthew Jennis ◽  
Cassandre R. Cavanaugh ◽  
Wensheng Lang ◽  
Bhanu Singh ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Blood Glucose ◽  
Stress Response ◽  
Food Intake ◽  
Serine Protease ◽  
Plasma Levels ◽  
Metabolic Adaptation ◽  
Fibroblast Growth Factor 21 ◽  
Integrated Stress Response

Trypsin is the major serine protease responsible for intestinal protein digestion. An inhibitor, camostat (CS), reduced weight gain, hyperglycemia, and dyslipidemia in obese rats; however, the mechanisms for these are largely unknown. We reasoned that CS creates an apparent dietary protein restriction, which is known to increase hepatic fibroblast growth factor 21 (FGF21). Therefore, metabolic responses to CS and a gut-restricted CS metabolite, FOY-251, were measured in mice. Food intake, body weight, blood glucose, branched-chain amino acids (LC/MS), hormone levels (ELISA), liver pathology (histology), and transcriptional changes (qRT-PCR) were measured in ob/ob, lean and diet-induced obese (DIO) C57BL/6 mice. In ob/ob mice, CS in chow (9–69 mg/kg) or FOY-251 (46 mg/kg) reduced food intake and body weight gain to a similar extent as pair-fed mice. CS decreased blood glucose, liver weight, and lipidosis and increased FGF21 gene transcription and plasma levels. In lean mice, CS increased liver FGF21 mRNA and plasma levels. Relative to pair feeding, FOY-251 also increased plasma FGF21 and induced liver FGF21 and integrated stress response (ISR) transcription. In DIO mice, FOY-251 (100 mg/kg po) did not alter peak glucose levels but reduced the AUC of the glucose excursion in response to an oral glucose challenge. FOY-251 increased plasma FGF21 levels. In addition to previously reported satiety-dependent (cholecystokinin-mediated) actions, intestinal trypsin inhibition engages non-satiety-related pathways in both leptin-deficient and DIO mice. This novel mechanism improves metabolism by a liver-integrated stress response and increased FGF21 expression levels in mice. NEW & NOTEWORTHY Trypsin inhibitors, including plant-based consumer products, have long been associated with metabolic improvements. Studies in the 1980s and 1990s suggested this was due to satiety hormones and caloric wasting by loss of protein and fatty acids in feces. This work suggests an entirely new mechanism based on the lower amounts of digested protein available in the gut. This apparent protein reduction may cause beneficial metabolic adaptation by the intestinal-liver axis to perceived nutrient stress.

scholarly journals Urocortin 2 acts centrally to delay gastric emptying through sympathetic pathways while CRF and urocortin 1 inhibitory actions are vagal dependent in rats

2006 ◽  
Vol 290 (3) ◽  
pp. G511-G518 ◽  
Author(s):  
József Czimmer ◽  
Mulugeta Million ◽  
Yvette Taché
Keyword(s):  
Gastric Emptying ◽  
Receptor Agonist ◽  
Inhibitory Action ◽  
Delayed Gastric Emptying ◽  
Inhibitory Effect ◽  
Corticotropin Releasing Factor ◽  
Phenol Red ◽  
Sympathetic Blockade ◽  
Intracisternal Injection ◽  
Urocortin 1

We characterized the influence of the selective corticotropin-releasing factor 2 (CRF2) receptor agonist human urocortin 2 (Ucn 2), injected intracisternally, on gastric emptying and its mechanism of action compared with intracisternal CRF or urocortin (Ucn 1) in conscious rats. The methylcellulose phenol red solution was gavaged 20 min after peptide injection, and gastric emptying was measured 20 min later. The intracisternal injection of Ucn 2 (0.1 and 1 μg) and Ucn 1 (1 μg) decreased gastric emptying to 37.8 ± 6.9%, 23.1 ± 8.6%, and 21.6 ± 5.9%, respectively, compared with 58.4 ± 3.8% after intracisternal vehicle. At lower doses, Ucn 2 (0.03 μg) and Ucn 1 (0.1 μg) had no effect. The CRF2 antagonist astressin2-B (3 μg ic) antagonized intracisternal Ucn 2 (0.1 μg) and CRF (0.3 μg)-induced inhibition of gastric emptying. Vagotomy enhanced intracisternal Ucn 2 (0.1 or 1 μg)-induced inhibition of gastric emptying compared with sham-operated group, whereas it blocked intracisternal CRF (1 μg) inhibitory action (45.5 ± 8.4% vs. 9.7 ± 9.7%). Sympathetic blockade by bretylium prevented intracisternal and intracerebroventricular Ucn 2-induced delayed gastric emptying, whereas it did not influence intravenous Ucn 2-, intracisternal CRF-, and intracisternal Ucn 1-induced inhibition of gastric emptying. Prazosin abolished the intracisternal Ucn 2 inhibitory effect, whereas yohimbine and propranolol did not. None of the pretreatments modified basal gastric emptying. These data indicate that intracisternal Ucn 2 induced a central CRF2-mediated inhibition of gastric emptying involving sympathetic α1-adrenergic mechanisms independent from the vagus contrasting with the vagal-dependent inhibitory actions of CRF and Ucn 1.

scholarly journals Postgraduate Symposium The role of fat in gastric emptying and satiety: acute and chronic effects

2009 ◽  
Vol 68 (1) ◽  
pp. 89-97 ◽  
Author(s):  
Miriam Clegg ◽  
Amir Shafat
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Gastrointestinal Transit ◽  
Positive Energy ◽  
Low Fat ◽  
Low Fat Diet ◽  
The Metabolic Syndrome ◽  
Increase Food Intake ◽  
Positive Energy Balance

Dietary fat is an important factor in the aetiology of obesity and the metabolic syndrome. It has been widely debated whether gastric emptying (GE) is altered in obesity. GE times have been reported as both longer and shorter in obese individuals compared with matched lean individuals. However, the general consensus is that GE is accelerated and satiety is lower in obesity. Research has implicated a high-fat (HF) diet in these findings. A single HF meal has a longer GE time than a low-fat meal and can even delay GE of the subsequent meal. However, an HF diet has shown different effects. Feeding a HF diet adapts gastrointestinal function to reduce GE times in comparison with a low-fat diet. Increased GE may lead to decreased satiety and faster onset of subsequent eating episodes. Further results have suggested that consuming an HF diet for 14 d increases the GE rate of HF food but not low-fat food. Consuming HF diets for 2 weeks has also been shown to increase food intake. Decreased satiation following an HF diet may cause increased food intake and a positive energy balance, potentially resulting in a gradual increase in adiposity. Recent results have suggested that gastrointestinal transit is accelerated following only 3 d on a HF diet. The variable GE times reported in obesity may be associated with interactions between the HF diet and obesity and not simply the obese state.

Cocaine and exercise: temporal changes in plasma levels of catecholamines, lactate, glucose, and cocaine

1996 ◽  
Vol 270 (3) ◽  
pp. E438-E444 ◽  
Author(s):  
D. H. Han ◽  
K. P. Kelly ◽  
G. W. Fellingham ◽  
R. K. Conlee
Keyword(s):  
Blood Glucose ◽  
Intravenous Injection ◽  
Plasma Levels ◽  
Half Life ◽  
Venous Blood ◽  
Combined Effect ◽  
Plasma Epinephrine ◽  
Blood Samples ◽  
Treatment Groups ◽  
Elimination Half

To determine the combined sympathoadrenal effects of cocaine and exercise in awake animals, rats were assigned to one of four treatment groups: saline-rest (SR), saline-exercise (SE), cocaine-rest (CR), and cocaine-exercise (CE). Venous blood samples from jugular catheters were obtained at -40, 0-4, 7, 10, 13, 16, 19, 26, and 36 min after intravenous injection of cocaine (5 mg/kg) or saline and the simultaneous onset of a 16-min treadmill run (26 m/min, 10% grade). CE increased plasma epinephrine (24.2 nM at 16 min), norepinephrine (28.0 nM at 10 min), and lactate (11.2 mM at 4 min) to levels 2-5 times greater than either treatment (SE and CR) alone (P<0.05) and 11-35 times higher that SR. Blood glucose values were significantly depressed in CE (-33% vs. SE) but increased in CR (+26% vs. SR). Plasma cocaine peaked < 2 min after injection in both CR and CE, and the peak was 69% higher in CE (P<0.05); however, the plasma elimination half-life (12-14 min) was not different. These results indicate that the combined effect of the two sympathoadrenal stimulants, exercise and cocaine, amplify the catecholamine responses to levels far greater than when each stimulant is used alone.

Sign in / Sign up

Export Citation Format

Share Document