scholarly journals The effects of pregnancy and lactation on the activities of trypsin and α-chymotrypsin in the rat pancreas

1979 ◽  
Vol 41 (3) ◽  
pp. 573-578 ◽  
Author(s):  
B. A. Rolls ◽  
M. J. Henschel ◽  
Maureen F. Palmer
Keyword(s):  
Insulin Secretion ◽  
Food Intake ◽  
Nutrient Availability ◽  
Gut Hormones ◽  
Weaning Food ◽  
Rat Pancreas ◽  
Trophic Effects ◽  
Chymotrypsin Activity ◽  
Pregnancy And Lactation ◽  
Pancreas Weight

1. The food intake, pancreas weight and trypsin (EC 3.4.21.4) and α-chymotrypsin (EC 3.4.21.1) activities in the pancreas were measured in rats during pregnancy and lactation and after the young were weaned.2. All the quantities measured increased significantly during lactation and had returned to their original values by 4 weeks after weaning. Food intake and pancreas weight were highest after the second week of lactation. Total trypsin and α-chymotrypsin activity, and the activity per g tissue, fell during pregnancy and rose during lactation, reaching a maximum I week after weaning.3. From these and other results it is suggested that the hypertrophy and hypersecretion of pregnancy and lactation are initiated by changes in insulin secretion and mediated by the trophic effects of gut hormones, and that differences in the nature and timing of the response may be controlled by nutrient availability.

scholarly journals Changes in mRNA expression of arcuate nucleus appetite-regulating peptides during lactation in rats

2013 ◽  
Vol 52 (2) ◽  
pp. 97-109 ◽  
Author(s):  
Yoshihiro Suzuki ◽  
Keiko Nakahara ◽  
Keisuke Maruyama ◽  
Rieko Okame ◽  
Takuya Ensho ◽  
...  
Keyword(s):  
Food Intake ◽  
Mrna Expression ◽  
Arcuate Nucleus ◽  
Peptide Yy ◽  
Weaning Food ◽  
Hypothalamic Arcuate Nucleus ◽  
Pregnancy And Lactation ◽  
Acyl Ghrelin ◽  
Plasma Leptin ◽  
Agouti Related Protein

The contribution of hypothalamic appetite-regulating peptides to further hyperphagia accompanying the course of lactation in rats was investigated by using PCR array and real-time PCR. Furthermore, changes in the mRNA expression for appetite-regulating peptides in the hypothalamic arcuate nucleus (ARC) were analyzed at all stages of pregnancy and lactation, and also after weaning. Food intake was significantly higher during pregnancy, lactation, and after weaning than during non-lactation periods. During lactation, ARC expression of mRNAs for agouti-related protein (AgRP) and peptide YY was increased, whereas that of mRNAs for proopiomelanocortin (POMC) and cholecystokinin (CCK) was decreased, in comparison with non-lactation periods. The increase in AgRP mRNA expression during lactation was especially marked. The plasma level of leptin was significantly decreased during the course of lactation, whereas that of acyl-ghrelin was unchanged. In addition, food intake was negatively correlated with the plasma leptin level during lactation. This study has clarified synchronous changes in the expression of many appetite-regulating peptides in ARC of rats during lactation. Our results suggest that hyperphagia during lactation in rats is caused by decreases in POMC and CCK expression and increases in AgRP expression in ARC, the latter being most notable. Together with the decrease in the blood leptin level, such changes in mRNA expression may explain the further hyperphagia accompanying the course of lactation.

Effect of somatostatin-28 on dynamics of insulin secretion in perfused rat pancreas

Diabetes ◽  
1991 ◽  
Vol 40 (9) ◽  
pp. 1163-1169 ◽  
Author(s):  
J. W. Ensinck ◽  
E. C. Laschansky ◽  
R. E. Vogel ◽  
D. A. D'Alessio
Keyword(s):  
Insulin Secretion ◽  
Perfused Rat Pancreas ◽  
Rat Pancreas ◽  
Dynamics Of Insulin Secretion

Inhibition of Glucagon and Insulin Secretion by Somatostatin in the Rat Pancreas Perfusedin Situ

Endocrinology ◽  
1975 ◽  
Vol 96 (2) ◽  
pp. 370-374 ◽  
Author(s):  
D. G. JOHNSON ◽  
J. W ENSINCK ◽  
D. KOERKER ◽  
J. PALMER ◽  
J. GOODNER
Keyword(s):  
Insulin Secretion ◽  
Rat Pancreas ◽  
Glucagon And Insulin

Secretin as a satiation whisperer with the potential to turn into an obesity-curbing knight

Endocrinology ◽  
2021 ◽  
Author(s):  
Katharina Schnabl ◽  
Yongguo Li ◽  
Mueez U-Din ◽  
Martin Klingenspor
Keyword(s):  
Bariatric Surgery ◽  
Body Weight ◽  
Energy Balance ◽  
Food Intake ◽  
Weight Control ◽  
Therapeutic Potential ◽  
Physiological Mechanism ◽  
Gut Hormones ◽  
Metabolic Effects ◽  
Beneficial Effects

Abstract The obesity pandemic requires effective preventative and therapeutic intervention strategies. Successful and sustained obesity treatment is currently limited to bariatric surgery. Modulating the release of gut hormones is considered promising to mimic bariatric surgery with its beneficial effects on food intake, body weight and blood glucose levels. The gut peptide secretin was the first molecule to be termed a hormone; nevertheless, it only recently has been established as a legitimate anorexigenic peptide. In contrast to gut hormones that crosstalk with the brain either directly or by afferent neuronal projections, secretin mediates meal-associated brown fat thermogenesis to induce meal termination, thereby qualifying this physiological mechanism as an attractive, peripheral target for the treatment of obesity. In this perspective, it is of pivotal interest to deepen our yet superficial knowledge on the physiological roles of secretin as well as meal-associated thermogenesis in energy balance and body weight regulation. Of note, the emerging differences between meal-associated thermogenesis and cold-induced thermogenesis must be taken into account. In fact, there is no correlation between these two entities. In addition, the investigation of potential effects of secretin in hedonic-driven food intake, bariatric surgery as well as chronic treatment using suitable application strategies to overcome pharmacokinetic limitations will provide further insight into its potential to influence energy balance. The aim of this article is to review the facts on secretin’s metabolic effects, address prevailing gaps in our knowledge, and provide an overview on the opportunities and challenges of the therapeutic potential of secretin in body weight control.

Limits to sustained energy intake

2001 ◽  
Vol 204 (11) ◽  
pp. 1947-1956 ◽  
Author(s):  
M. S. Johnson ◽  
S. C. Thomson ◽  
J. R. Speakman
Keyword(s):  
Food Intake ◽  
Energy Intake ◽  
Litter Size ◽  
Resting Metabolic Rate ◽  
Control Group ◽  
Lower Mass ◽  
Daily Food Intake ◽  
Energy Demands ◽  
Daily Food ◽  
Pregnancy And Lactation

SUMMARYTo determine whether mice were limited in their capacity to absorb energy during late lactation, we attempted to increase the energy burden experienced by a group of female mice during late lactation by mating them at the postpartum oestrus, hence combining the energy demands of pregnancy and lactation. These experimental mice were therefore concurrently pregnant and lactating in their first lactation, and were followed through a normal second lactation. In a control group, females also underwent two lactations but sequentially, with the second mating after the first litter had been weaned. Maternal mass and food intake were measured throughout the first lactation, second pregnancy and second lactation. Maternal resting metabolic rate (RMR) was measured prior to the first mating and then at the peak of both the first and second lactations. Litter size and litter mass were also measured throughout both lactations. In the first lactation, experimental mice had a lower mass-independent RMR (F1,88=5.15, P=0.026) and raised significantly heavier pups (t=2.77, d.f.=32, P=0.0093) than the control mice. Experimental mice delayed implantation at the start of the second pregnancy. The extent of the delay was positively related to litter size during the first lactation (F1,19=4.58, P=0.046) and negatively related to mean pup mass (F1,19=5.78, P=0.027) in the first lactation. In the second lactation, the experimental mice gave birth to more (t=2.75, d.f.=38, P=0.0092) and lighter (t=−5.01, d.f.=38, P<0.0001) pups than did the controls in their second lactation. Maternal asymptotic daily food intake of control mice in the second lactation was significantly higher (t=−4.39, d.f.=37, P=0.0001) than that of the experimental mice and higher than that of controls during their first lactation. Despite the added burden on the experimental females during their first lactation, there was no increase in their food intake, which suggested that they might be limited by their capacity to absorb energy. However, control females appeared to be capable of increasing their asymptotic food intake beyond the supposed limits estimated previously, suggesting that the previously established limit was not a fixed central limitation on food intake. As RMR increased in parallel with the increase in food intake during the second lactation of control mice, the sustained energy intake remained at around 7.0×RMR.

scholarly journals Effects of sleeve gastrectomy and ileal transposition, alone and in combination, on food intake, body weight, gut hormones, and glucose metabolism in rats

2013 ◽  
Vol 305 (4) ◽  
pp. E507-E518 ◽  
Author(s):  
S. Nausheen ◽  
I. H. Shah ◽  
A. Pezeshki ◽  
D. L. Sigalet ◽  
P. K. Chelikani
Keyword(s):  
Body Weight ◽  
Sleeve Gastrectomy ◽  
Weight Gain ◽  
Food Intake ◽  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Gut Hormones ◽  
Ileal Transposition ◽  
Gastric Restriction ◽  
Peripheral Tissues

Bariatric surgeries are hypothesized to produce weight loss and improve diabetes control by multiple mechanisms including gastric restriction and lower gut stimulation; the relative importance of these mechanisms remains poorly understood. We compared the effects of a typical foregut procedure, sleeve gastrectomy, (SG) with a primarily hindgut surgery, ileal transposition (IT), alone and together (SGIT), or sham manipulations, on food intake, body weight, gut hormones, glucose tolerance, and key markers of glucose homeostasis in peripheral tissues of adult male Sprague-Dawley rats (450–550 g, n = 7–9/group). SG, IT, and SGIT surgeries produced transient reduction in food intake and weight gain; the effects of SG and IT on intake and body weight were nonadditive. SG, IT, and SGIT surgeries resulted in increased tissue expression and plasma concentrations of the lower gut hormones glucagon-like peptide-1 and peptide YY and decreased plasma glucose-dependent insulinotropic peptide, insulin, and leptin concentrations. Despite transient effects on intake and weight gain, the SG, IT, and SGIT surgeries produced a significant improvement in glucose tolerance. In support of glycemic improvements, the protein abundance of key markers of glucose metabolism (e.g., GLUT4, PKA, IRS-1) in muscle and adipose tissue were increased, whereas the expression of key gluconeogenic enzyme in liver (G-6-Pase) were decreased following the surgeries. Therefore, our data suggest that enhanced lower gut stimulation following SG, IT, and SGIT surgeries leads to transient reduction in food intake and weight gain together with enhanced secretion of lower gut hormones and improved glucose clearance by peripheral tissues.

RELEASE OF IMMUNOREACTIVE AND RADIOACTIVELY PRELABELLED ENDOGENOUS (PRO-)INSULIN FROM ISOLATED ISLETS OF RAT PANCREAS IN THE PRESENCE OF EXOGENOUS INSULIN

1977 ◽  
Vol 74 (2) ◽  
pp. 243-249 ◽  
Author(s):  
H. SCHATZ ◽  
E. F. PFEIFFER
Keyword(s):  
Insulin Secretion ◽  
Insulin Release ◽  
Feedback Mechanism ◽  
Isolated Islets ◽  
Immunoreactive Insulin ◽  
Hormone Release ◽  
Exogenous Insulin ◽  
Rat Pancreas ◽  
Direct Feedback

To study the influence of insulin on its own secretion, collagenase-isolated islets of rat pancreas were prelabelled with [3H]leucine for 2 h. After washing the islets, (pro-)insulin release was stimulated by glucose in the presence or absence of exogenous insulin (up to 2·5 mu./ml). Hormone release was unchanged by the presence of exogenous insulin as judged by determination of both immunoreactive insulin and radioactivity incorporated into the proinsulin and insulin fractions of the medium. No direct feedback mechanism for insulin secretion was apparent from this study.

Sign in / Sign up

Export Citation Format

Share Document