scholarly journals Functional changes of the small intestine in over- and undernourished suckling rats support the development of obesity risk on a high-energy diet in later life

2007 ◽  
pp. 183-192
Author(s):  
š Mozeš ◽  
z Šefčíková ◽  
Ľ Lenhardt
Keyword(s):  
Body Fat ◽  
Later Life ◽  
High Energy ◽  
Experimental Models ◽  
Obesity Risk ◽  
Sprague Dawley ◽  
Functional Changes ◽  
Caloric Density ◽  
Sprague Dawley Rats ◽  
Small Intestinal

To investigate the relationship between early nutritional experience, ontogeny of the small intestinal functions and predisposition to obesity development, the following experimental models of male Sprague-Dawley rats were used: 1) rats in which the quantity of nutrition was manipulated from birth to weaning (day 30) by adjusting the number of pups in the nest to 4 (SL), 10 (NL) and 16 pups (LL) and 2) littermates of SL, NL and LL rats fed either a standard or a hypercaloric diet from days 80 to 135 of age. The overfed SL pups were overweight after day 15 and became permanently obese, whereas the underfed smaller LL pups, due to accelerated growth and enhanced food intake from day 30 to day 35, attained a body fat level that did not differ from normally fed NL rats. Moreover, a significantly increased duodenal and jejunal alkaline phosphatase (AP) activity was found in SL and LL rats and these acquired somatic and intestinal characteristics persisted from weaning throughout life. Eight weeks of high-energy diet feeding elicited a similar pattern of intestinal response in SL and LL rats that was clearly different from NL rats. Despite energy over-consumption in these three groups, both SL and LL rats still displayed enhanced AP activity and showed a significant increase in protein/DNA ratio accompanied with a significant body fat accretion. These results indicate that the postnatally acquired small intestinal changes induced by over- and undernutrition could be involved in the similar predisposition to obesity risk in later life when caloric density of the diet is raised.

Resistance to Dietary Obesity in Rats Given Different High-Energy Diets

2006 ◽  
Vol 76 (5) ◽  
pp. 271-279 ◽  
Author(s):  
Pérez de Heredia ◽  
Garaulet ◽  
Puy Portillo ◽  
Zamora
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Body Fat ◽  
High Fat Diet ◽  
Wistar Rats ◽  
High Energy ◽  
Sprague Dawley ◽  
High Fat ◽  
Sprague Dawley Rats ◽  
Dietary Obesity

Susceptibility to dietary obesity was studied in Wistar and Sprague-Dawley rats submitted to different high-energy diets. Experiment 1: female Sprague-Dawley rats were fed chow (n = 6) or a high-fat diet (n = 12) for 22 weeks. Experiment 2: Wistar rats were fed chow or a high-fat diet, and Sprague-Dawley rats were given chow, high-fat, sweet condensed milk, or cafeteria diets, for eight weeks (6 animals per group). Food intake and body weight were recorded weekly. Adipose tissue was collected from periovarian, mesenteric, and subcutaneous regions and adipocytes were isolated and measured. Both strains showed similar energy intake and body weight gain. Wistar rats reached greater final body fat contents than Sprague-Dawley rats, regardless of the type of diet. However, resistance to dietary obesity was found in 100% of cases in both experiments. None of the diets succeeded in increasing body fat accumulation when compared to control groups. All adipose tissue locations were equally unaffected, with periovarian fat cells being larger than those in mesenteric and subcutaneous regions in all the groups. In view of the strong resistance to obesity observed in rats, it should be important for researchers to transmit the difficulties of inducing dietary obesity in these animals, in order to prevent bias in science interpretation.

Dietary Calcium Had No Reducing Effect on Body Fat and Weight Gain in Sprague-Dawley Rats

2007 ◽  
Vol 6 (5) ◽  
pp. 478-484 ◽  
Author(s):  
J.M. Malekzadeh ◽  
S.A. Keshavarz ◽  
F. Siassi ◽  
M. Eshraghian ◽  
M. Kadkhodaee ◽  
...  
Keyword(s):  
Weight Gain ◽  
Body Fat ◽  
Dietary Calcium ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

Behavioral and endocrine traits of obesity-prone and obesity-resistant rats on macronutrient diets

1998 ◽  
Vol 274 (6) ◽  
pp. E1057-E1066 ◽  
Author(s):  
Jian Wang ◽  
Jesline T. Alexander ◽  
Ping Zheng ◽  
Hi Joon Yu ◽  
Jordan Dourmashkin ◽  
...  
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Body Fat ◽  
High Fat Diet ◽  
Body Weight Gain ◽  
Normal Weight ◽  
Fat Intake ◽  
Sprague Dawley ◽  
Glucose Levels ◽  
Sprague Dawley Rats

Patterns of eating behavior, body weight gain, and hormone changes were examined in normal-weight albino Sprague-Dawley rats on macronutrient diets. These diets consisted of either three separate jars with pure macronutrients, fat, carbohydrate and protein, from which to choose, or a single diet with different concentrations of fat and carbohydrate. Similar patterns on the choice-diet and single-diet paradigms were observed. During the first 7–10 days on these diets but not subsequently, the rats consuming a fat-rich diet exhibit significant hyperphagia, an increase in both total and fat intake that produces higher body weight gain. Compared with a 10% fat diet, a 30% fat diet is associated with a decline in insulin and corticosterone (CORT) levels, whereas a 60% fat diet produces an increase in circulating glucose. Levels of glucose are positively correlated with fat intake, and together these measures are consistently related to body fat. These relationships are most strongly expressed in rats that consume a fat-rich diet with >30% fat. Whereas insulin levels are also positively related to body fat, CORT is inversely related in these normal-weight subjects. In animals consuming a high-fat diet, a clear separation can be seen between “obesity-prone” (OP) rats with 100% greater body fat than “obesity-resistant” (OR) rats. The OP rats, which consume 15% more total calories, have significantly higher insulin and glucose levels. In animals that consume a diet with >30% fat, it is the OP but not the OR rats that exhibit a positive relation between fat intake, glucose levels, and body fat and reveal an additional association between carbohydrate intake, insulin, and body fat. Thus these rats on macronutrient diets exhibit distinct traits that relate behavior to hormone disturbances and adiposity and distinguish subjects that are prone vs. resistant to obesity.

scholarly journals Effects of realimentation on small intestinal morphology and disaccharidase activity in malnutrition Sprague-Dawley rats

2006 ◽  
pp. 208
Author(s):  
Rustadi Sosrosumihardjo ◽  
Agus Firmansyah ◽  
Asri Rasad ◽  
Daldiyono Harjodisastro ◽  
Endi Ridwan ◽  
...  
Keyword(s):  
Intestinal Morphology ◽  
Sprague Dawley ◽  
Disaccharidase Activity ◽  
Sprague Dawley Rats ◽  
Small Intestinal

Ontogeny of diet-induced obesity in selectively bred Sprague-Dawley rats

2003 ◽  
Vol 285 (3) ◽  
pp. R610-R618 ◽  
Author(s):  
Matthew R. Ricci ◽  
Barry E. Levin
Keyword(s):  
Leptin Receptor ◽  
Splice Variants ◽  
Caloric Intake ◽  
High Energy ◽  
Sprague Dawley ◽  
Low Fat Diet ◽  
Diet Induced Obesity ◽  
Leptin Sensitivity ◽  
Sprague Dawley Rats ◽  
Plasma Leptin

Outbred Sprague-Dawley rats selectively bred for their propensity to develop diet-induced obesity (DIO) become heavier on low-fat diet than those bred to be diet resistant (DR) beginning at ∼5 wk of age. Here we assessed the development of metabolic and neural functions for insights into the origins of their greater weight gain. From week 5 to week 10, chow-fed DIO rats gained 15% more body weight and ate ∼14% more calories but had only slightly greater adiposity and plasma leptin than DR rats. From day 3 through week 10, DIO and DR rats had similar mRNA expression of arcuate nucleus neuropeptide Y, proopiomelanocortin, agouti-related peptide, and all splice variants of the leptin receptor (OB-R). When fed a high-energy (HE; 31% fat) diet, 7-wk-old DIO rats had a 240% increase in plasma leptin levels after only 3 days. Despite this early leptin rise, they maintained a persistent hyperphagia and became more obese than chow-fed DIO rats and DR rats fed chow or HE diet. Their failure to reduce caloric intake, despite high levels of leptin, suggests that selectively bred DIO rats might have reduced leptin sensitivity similar to that seen in the outbred DIO parent strain.

scholarly journals Hyperosmolarity in the small intestine contributes to postprandial ghrelin suppression

2014 ◽  
Vol 306 (12) ◽  
pp. G1108-G1116 ◽  
Author(s):  
Joost Overduin ◽  
Tracy S. Tylee ◽  
R. Scott Frayo ◽  
David E. Cummings
Keyword(s):  
Small Intestine ◽  
Glucose Solution ◽  
Jugular Vein ◽  
Gastric Bypass Surgery ◽  
Sprague Dawley ◽  
Macronutrient Composition ◽  
Sprague Dawley Rats ◽  
Small Intestinal ◽  
The Impact ◽  
Dietary Modifications

Plasma levels of the orexigenic hormone ghrelin are suppressed by meals with an efficacy dependent on their macronutrient composition. We hypothesized that heterogeneity in osmolarity among macronutrient classes contributes to these differences. In three studies, the impact of small intestinal hyperosmolarity was examined in Sprague-Dawley rats. In study 1, isotonic, 2.5×, and 5× hypertonic solutions of several agents with diverse absorption and metabolism properties were infused duodenally at a physiological rate (3 ml/10 min). Jugular vein blood was sampled before and at 30, 60, 90, 120, 180, 240, and 300 min after infusion. Plasma ghrelin was suppressed dose dependently and most strongly by glucose. Hyperosmolar infusions of lactulose, which transits the small intestine unabsorbed, and 3- O-methylglucose (3- O-MG), which is absorbed like glucose but remains unmetabolized, also suppressed ghrelin. Glucose, but not lactulose or 3- O-MG, infusions increased plasma insulin. In study 2, intestinal infusions of hyperosmolar NaCl suppressed ghrelin, a response that was not attenuated by coinfusion with the neural blocker lidocaine. In study 3, we reconfirmed that the low-osmolar lipid emulsion Intralipid suppresses ghrelin more weakly than isocaloric (but hypertonic) glucose. Importantly, raising Intralipid's osmolarity to that of the glucose solution by nonabsorbable lactulose supplementation enhanced ghrelin suppression to that seen after glucose. Hyperosmolar ghrelin occurred particularly during the initial 3 postinfusion hours. We conclude that small intestinal hyperosmolarity 1) is sufficient to suppress ghrelin, 2) may combine with other postprandial mechanisms to suppress ghrelin, 3) might contribute to altered ghrelin regulation after gastric bypass surgery, and 4) may inform dietary modifications for metabolic health.

scholarly journals Identification of transient glycosylation alterations of sialylated mucin oligosaccharides during infection by the rat intestinal parasite Nippostrongylus brasiliensis

2000 ◽  
Vol 350 (3) ◽  
pp. 805-814 ◽  
Author(s):  
Niclas G. KARLSSON ◽  
Fredrik J. OLSON ◽  
Per-Åke JOVALL ◽  
Ylva ANDERSCH ◽  
Lennart ENERBÄCK ◽  
...  
Keyword(s):  
Infection Process ◽  
Nippostrongylus Brasiliensis ◽  
Blood Group Antigens ◽  
Intestinal Infection ◽  
Sprague Dawley ◽  
Acetylneuraminic Acid ◽  
Sprague Dawley Rats ◽  
Small Intestinal ◽  
Infectious Cycle ◽  
Intestinal Mucins

The sialylation of the oligosaccharides from small-intestinal mucins during a 13-day infectious cycle was studied in Sprague–Dawley rats with the parasite Nippostrongylus brasiliensis. Sialic acid analysis and release, permethylation and analysis by GC-MS of the sialylated oligosaccharides isolated from the ‘insoluble’ mucin complex revealed a relative decrease (4–7-fold) of N-glycolylneuraminic acid compared with N-acetylneuraminic acid just before parasite expulsion. Northern blots showed that this effect was due to the decreased expression of a hydroxylase converting CMP-N-acetylneuraminic acid into CMP-N-glycolylneuraminic acid. Analysis of other rat strains showed that this parasite infection also caused the same effect in these animals. Detailed analysis of infected Sprague–Dawley rats revealed four sialylated oligosaccharides not found in the uninfected animals. These new oligosaccharides were characterized in detail and all shown to contain the trisaccharide epitope NeuAc/NeuGcα2-3(GalNAcβ1-4)Galβ1 (where NeuGc is N-glycolyl neuraminic acid). This epitope is similar to the Sda- and Cad-type blood-group antigens and suggests that the infection causes the induction of a GalNAcβ1-4 glycosyltransferase. This model for an intestinal infection suggests that the glycosylation of intestinal mucins is a dynamic process being modulated by the expression of specific enzymes during an infection process.

scholarly journals Interaction of Manganese and Ammonia in the Brain of Hepatic Encephalopathy Rats

2020 ◽  
Vol 20 (8) ◽  
Author(s):  
Jingjing Lu ◽  
Ying Li ◽  
Cui Zhang ◽  
Xiuying Yang ◽  
Jin Wei Qiang
Keyword(s):  
Hepatic Encephalopathy ◽  
Glutamine Synthetase ◽  
Control Group ◽  
Blood Ammonia ◽  
Sprague Dawley ◽  
Rat Models ◽  
Functional Changes ◽  
Sprague Dawley Rats ◽  
Mn Content ◽  
The Brain

Background: Both ammonia and manganese (Mn) play a key role in the pathogenesis of hepatic encephalopathy (HE) and cause similar morphological and functional changes in astrocytes. Objectives: To investigate the interaction between brain Mn and ammonia in HE rats. Methods: Three rat models of minimal HE (MHE), chronic manganism (CHM), and chronic hyperammonemia (CHA) were constructed. A total of 48 Sprague-Dawley rats were divided into one control group (n = 6), MHE groups (n = 18, among which six rats were used to evaluate the MHE model), CHM groups (n = 12), and CHA groups (n = 12). The CHM, CHA, and the rest of MHE rats were randomly divided further into two subgroups, according to the MgSO4 treatment (oral administration of 496 mg/kg/day for seven weeks): MHE-7W and MHE + Mg-7W; CHM-7W and CHM + Mg-7W; and CHA-7W and CHA + Mg-7W, respectively. Rats’ blood ammonia, brain Mn, glutamine synthetase (GS), and glutamine (GLN) levels were measured and compared among groups. Results: Significantly higher brain Mn content in MHE-7W and CHM-7W rats, higher blood ammonia levels, brain GS activity, and GLN content were observed in MHE-7W, CHM-7W, and CHA-7W rats than in control rats. After MgSO4 treatment for seven weeks, significantly lower brain Mn content, blood ammonia levels, and GLN content were observed in MHE, CHM, and CHA rats. Conclusions: Our study showed that brain Mn accumulation could increase brain ammonia levels, while the accumulation of brain ammonia had no effect on the content of brain Mn.

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