scholarly journals Long-term consequences of under-nutrition during suckling on glucose tolerance and lipoprotein profile in female and male rats

2006 ◽  
Vol 96 (6) ◽  
pp. 1030-1037 ◽  
Author(s):  
Iliana López-Soldado ◽  
Maria Angeles Munilla ◽  
Emilio Herrera
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Cell Function ◽  
Male Rats ◽  
Epididymal Adipose Tissue ◽  
Oral Glucose ◽  
Standard Diet ◽  
Sprague Dawley ◽  
Under Nutrition ◽  
Β Cell Function

To determine the effect of under-nutrition during suckling in adults, at delivery female Sprague Dawley rats were allowed to lactate litters of either eight (controls) or sixteen pups each (large litter, LL). The amount of milk taken by LL pups was less than the controls and the concentration of triacylglycerols (TG) in the milk of the former was lower. The increase of both body weight and length in LL was lower than in the controls during suckling. At weaning, pups were allowed to eat ad libitum a standard diet and whereas at 20 months female body weight did not differ between LL and control rats, LL males weighed less than controls. Plasma NEFA were lower in male LL than in controls at 10 months, leptin at 10 and 16 months and TG and VLDL-TG at 20 months, with no differences in females. When 20 months old, lumbar and epididymal adipose tissue weights were lower in male LL than in controls, but not in females. The increase in plasma insulin after oral glucose load was lower in LL than in controls, both in males and females at 4 and 16 months, and only in males at 10 months, whereas the change in plasma glucose remained constant between the groups. Results indicate that both the pancreatic β-cell function and insulin sensitivity and adipose tissue metabolism are independently programmed as a consequence of under-nutrition during suckling, the effect being more manifest for males than for females.

scholarly journals Carbohydrate-Responsive Gene Expression in the Adipose Tissue of Rats

Endocrinology ◽  
2010 ◽  
Vol 151 (1) ◽  
pp. 153-164 ◽  
Author(s):  
Kartik Shankar ◽  
Amanda Harrell ◽  
Ping Kang ◽  
Rohit Singhal ◽  
Martin J. J. Ronis ◽  
...  
Keyword(s):  
Gene Expression ◽  
Body Composition ◽  
Body Weight ◽  
Adipose Tissue ◽  
Body Weight Gain ◽  
Caloric Intake ◽  
Oral Glucose ◽  
Sprague Dawley ◽  
Simple Carbohydrates ◽  
The Impact

Abstract Although obesity is often associated with high-fat diets, it can develop from a variety of meal patterns. Excessive intake of simple carbohydrates is one consistent eating behavior leading to obesity. However, the impact of overconsumption of diets with high carbohydrate to fat ratios (C/F) on body composition and global adipose tissue gene expression remains unclear. We used total enteral nutrition to evaluate the effects of caloric intake and C/F on body weight gain and development of obesity. Female Sprague Dawley rats were fed diets with either low C/F or high C/F (HC) (reflecting a 19.5-fold increase in C/F) at two levels of caloric intake: 187 or 220 kcal/kg3/4 · d (15% excess) for 4 wk. At the end of the study period, rats fed HC diets had about 20% higher body weight at either caloric intake compared with rats fed low C/F diets (P < 0.05). Body composition (assessed by nuclear magnetic resonance, computerized tomography, and adipose tissue weights) revealed higher percent fat mass (P < 0.05) in HC rats. Obesity was associated with increased serum resistin, leptin, fasting hyperinsulinemia, and insulin resistance after an oral glucose challenge (P < 0.05). Microarray analyses of adipose tissues revealed HC diets led to changes in 270 and 464 transcripts at 187 and 220 kcal/kg3/4 · d intakes. Genes regulating glucose transport, glycolysis, fatty acid and triglyceride biosynthesis, desaturation and elongation, adipogenesis, and adipokines were affected by HC diets. These results suggest that C/F and interactions with excessive caloric intake per se may regulate body composition and play important roles in the development of obesity and metabolic syndrome.

scholarly journals Antihyperglycemic Effects and Mode of Actions of Musa paradisiaca Leaf and Fruit Peel Hydroethanolic Extracts in Nicotinamide/Streptozotocin-Induced Diabetic Rats

2020 ◽  
Vol 2020 ◽  
pp. 1-15 ◽  
Author(s):  
Sarah M. Abdel Aziz ◽  
Osama M. Ahmed ◽  
Sanaa M. Abd EL-Twab ◽  
Hessah Mohammed Al-Muzafar ◽  
Kamal Adel Amin ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Intraperitoneal Injection ◽  
Cell Function ◽  
Elevated Serum ◽  
Diabetic Rats ◽  
Oral Glucose ◽  
Fruit Peel ◽  
Musa Paradisiaca ◽  
Peel Extract

The present study aimed to evaluate the antihyperglycemic effects of Musa paradisiaca (M. paradisiaca) leaf and fruit peel hydroethanolic extracts and to suggest their probable mode of actions in nicotinamide (NA)/streptozotocin (STZ)-induced diabetic rats. The leaf and fruit peel hydroethanolic extracts were analyzed by GC-MS that indicated the presence of phytol, octadecatrienoic acid, hexadecanoic acid, and octadecadienoic acid as major components in the leaf extract and vitamin E, octadecenamide, β-sitosterol, and stigmasterol as major phytochemicals in the fruit peel extract. Diabetes mellitus was induced by a single intraperitoneal injection of STZ (60 mg/kg body weight) dissolved in citrate buffer (pH 4.5), 15 minutes after intraperitoneal injection of NA (120 mg/kg body weight). The NA/STZ-induced diabetic rats were, respectively, treated with M. paradisiaca leaf and fruit peel hydroethanolic extracts at a dose of 100 mg/kg body weight/day by oral administration for 28 days. The treatment of NA/STZ-induced diabetic rats with leaf and fruit peel extracts significantly improved the impaired oral glucose tolerance and significantly increased the lowered serum insulin and C-peptide levels. The HOMA-IR (as the index of insulin resistance) and QUICKI (as a marker for insulin sensitivity), as well as HOMA-β cell function were significantly alleviated as a result of treatment of diabetic rats with leaf and fruit peel extracts. In association, the elevated serum-free fatty acids, TNF-α, and IL-6 levels were significantly decreased. In addition, the suppressed adipose tissue PPARγ, GLUT4, adiponectin, and insulin receptor β-subunit mRNA expressions were upregulated while the elevated adipose tissue resistin expression was downregulated in diabetic rats as a result of treatment with the leaf and peel extract. Based on these results, it can be concluded that M. paradisiaca leaf and fruit peel hydroethanolic extracts have antihyperglycemic effects which may be mediated via their insulinotropic and insulin-sensitizing effects.

scholarly journals Bacteroides uniformis CECT 7771 alleviates inflammation within the gut-adipose tissue axis involving TLR5 signaling in obese mice

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Emanuel Fabersani ◽  
Kevin Portune ◽  
Isabel Campillo ◽  
Inmaculada López-Almela ◽  
Sergio Montserrat-de la Paz ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Body Weight Gain ◽  
Western Diet ◽  
Lymphoid Cells ◽  
Epididymal Adipose Tissue ◽  
Oral Glucose ◽  
Standard Diet ◽  
Intestinal Bacterium ◽  
Metabolic Dysfunction ◽  
Obese Mice

AbstractThis study investigated the immune mechanisms whereby administration of Bacteroides uniformis CECT 7771 reduces metabolic dysfunction in obesity. C57BL/6 adult male mice were fed a standard diet or a Western diet high in fat and fructose, supplemented or not with B. uniformis CECT 7771 for 14 weeks. B. uniformis CECT 7771 reduced body weight gain, plasma cholesterol, triglyceride, glucose, and leptin levels; and improved oral glucose tolerance in obese mice. Moreover, B. uniformis CECT 7771 modulated the gut microbiota and immune alterations associated with obesity, increasing Tregs and reducing B cells, total macrophages and the M1/M2 ratio in both the gut and epididymal adipose tissue (EAT) of obese mice. B. uniformis CECT 7771 also increased the concentration of the anti-inflammatory cytokine IL-10 in the gut, EAT and peripheral blood, and protective cytokines TSLP and IL-33, involved in Treg induction and type 2 innate lymphoid cells activation, in the EAT. It also restored the obesity–reduced TLR5 expression in the ileum and EAT. The findings indicate that the administration of a human intestinal bacterium with immunoregulatory properties on the intestinal mucosa helps reverse the immuno-metabolic dysfunction caused by a Western diet acting over the gut-adipose tissue axis.

scholarly journals Maternal Chronodisruption Throughout Pregnancy Impairs Glucose Homeostasis and Adipose Tissue Physiology in the Male Rat Offspring

2021 ◽  
Vol 12 ◽  
Author(s):  
Diego Halabi ◽  
Hans G. Richter ◽  
Natalia Mendez ◽  
Thilo Kähne ◽  
Carlos Spichiger ◽  
...  
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Glucose Homeostasis ◽  
Body Weight Gain ◽  
Adult Life ◽  
Tissue Response ◽  
Female Rats ◽  
Male Rat ◽  
Standard Diet ◽  
Sprague Dawley

Compelling evidence in rats support the idea that gestational chronodisruption induces major changes in maternal circadian rhythms and fetal development and that these changes impact adult life at many physiological levels. Using a model of chronic photoperiod shifting throughout gestation (CPS), in which pregnant female rats (Sprague–Dawley strain; n = 16 per group) were exposed to lighting schedule manipulation every 3–4 days reversing the photoperiod completely or light/dark photoperiod (12/12; LD), we explored in the adult rat male offspring body weight gain, glucose homeostasis, adipose tissue content, adipose tissue response to norepinephrine (NE), and adipose tissue proteomic in the basal condition with standard diet (SD) and in response to high-fat diet (HFD). In adult CPS male (100–200 days old; n = 8 per group), we found increasing body weight, under SD and adiposity. Also, we found an increased response to intraperitoneal glucose (IGTT). After 12 weeks of HFD, white adipose tissue depots in CPS offspring were increased further, and higher IGTT and lower intraperitoneal insulin tolerance response were found, despite the lack of changes in food intake. In in vitro experiments, we observed that adipose tissue (WAT and BAT) glycerol response to NE from CPS offspring was decreased, and it was completely abolished by HFD. At the proteomic level, in CPS adipose tissue, 275 proteins displayed differential expression, compared with LD animals fed with a standard diet. Interestingly, CPS offspring and LD fed with HFD showed 20 proteins in common (2 upregulated and 18 downregulated). Based on these common proteins, the IPA analysis found that two functional pathways were significantly altered by CPS: network 1 (AKT/ERK) and network 2 (TNF/IL4; data are available via ProteomeXchange with identifier PXD026315). The present data show that gestational chronodisruption induced deleterious effects in adipose tissue recruitment and function, supporting the idea that adipose tissue function was programmed in utero by gestational chronodisruption, inducing deficient metabolic responses that persist into adulthood.

scholarly journals Effects of smoking cessation on β-cell function, insulin sensitivity, body weight, and appetite

2014 ◽  
Vol 170 (2) ◽  
pp. 219-227 ◽  
Author(s):  
Marietta Stadler ◽  
Larissa Tomann ◽  
Angela Storka ◽  
Michael Wolzt ◽  
Slobodan Peric ◽  
...  
Keyword(s):  
Smoking Cessation ◽  
Body Weight ◽  
Insulin Sensitivity ◽  
Cell Function ◽  
Oral Glucose ◽  
Smoking Abstinence ◽  
Fasting Insulin ◽  
Cell Secretion ◽  
Β Cell ◽  
Β Cell Function

ObjectiveTo stop smoking is commonly associated with significant weight gain, but the mechanisms for this are poorly understood. We assessed the effects of smoking cessation on body weight, insulin sensitivity, β-cell function, and appetite.Subjects and methodsTwenty-seven long-term smokers (n=27; nine females/18 males, 28±1 years, 22.9±0.6 kg/m2) attending an ambulatory smoking cessation program in a community hospital in Vienna, Austria were examined at baseline (Visit A; still smoking) and after a minimum of 3 months of smoking abstinence (Visit B;n=14); relapsed smokers were not followed up. Participants underwent 3-h oral glucose tolerance tests and body composition measurements at each study visit. Fasting (QUICKI) and dynamic (oral glucose insulin sensitivity (OGIS)) insulin sensitivity and β-cell secretion (insulinogenic index 140 (IGI40)) were calculated. Food intake was quantified with a free choice buffet. Fasting plasma concentrations of neuropeptide-Y (NPY), peptide-YY (PYY), glucagon-like peptide 1 (GLP1), leptin, ghrelin, and visfatin were measured.ResultsAfter >3 months' smoking abstinence, body weight, and fat mass were increased (+4 and +22% respectively,P<0.05) and fasting insulin sensitivity deteriorated (QUICKI: post, 0.37±0.02 vs baseline, 0.41±0.2;P<0.05), while OGIS remained unchanged throughout. IGI40 increased by 31% after >3 months' smoking abstinence (P<0.01). Carbohydrate ingestion increased after stopping smoking (P<0.05). NPY fasting levels were increased after >3 months (P<0.05), PYY, GLP1, leptin, ghrelin, and visfatin were unchanged.ConclusionSmoking cessation is associated with transient metabolic changes including increased β-cell secretion in response to glucose and fasting insulin resistance. These alterations may be associated with or contribute to the body weight gain after smoking cessation.

scholarly journals FRUCTOSE;

2018 ◽  
Vol 21 (01) ◽  
pp. 136-143
Author(s):  
Zehra Naz ◽  
Abdul Khaliq Naveed ◽  
Mehdi Raza
Keyword(s):  
Body Weight ◽  
Diet Group ◽  
Male Rats ◽  
Blood Levels ◽  
Standard Diet ◽  
Sprague Dawley ◽  
Group Iii ◽  
Long Run ◽  
Group I ◽  
Obesity Hypertension

Objectives: To study and compare the effects of fructose and galactose on, bloodglucose, insulin, HbA and lipids and anthropometric measurements. Data Source: Ninety, 1chealthy adult male rats of Sprague-Dawley strain. Design: Experimental study. Setting:Department of Biochemistry and Molecular Biology, A.M.C, Rawalpindi, in collaboration withN.I.H, Islamabad. Period: Twelve months. Subjects and Methods: Rats weighing 180-350 gramswere selected by random sampling and were divided into three groups, 30 each. Group I wasgiven standard diet, Group II was given high fructose diet (HFD), i.e., 1.5gms/Kg body weight/dayof fructose, along with standard diet for two weeks and Group III was given high galactose diet,i.e., 0.83gms/Kg body weight/day, along with standard diet for two weeks. Results: There was asignificant increase in height of galactose group while fructose group has significant weight loss;BMI decreased in both but more in former. The blood levels of cholesterol, HDL-c, LDL-c, TG, andinsulin were significantly higher in fructose group than in galactose group. There was nosignificant difference between blood glucose and HbA among these groups yet their higher 1clevels indicate the chances of developing insulin resistance. Conclusions: Fructose due to itsless hyperglycaemic effects should not be used in diet and must not be prescribed in diabetes, asin the long run it can lead to obesity, hypertension and cardiovascular risk. Non-significant effectsof galactose on above parameters (except lipoproteins), does not mean that it can be used as analternative to fructose and this area needs exploration.

scholarly journals Fetal androgen signaling defects affect pancreatic β-cell mass and function, leading to glucose intolerance in high-fat diet-fed male rats

2019 ◽  
Vol 317 (5) ◽  
pp. E731-E741 ◽  
Author(s):  
Naoki Harada ◽  
Yusuke Yotsumoto ◽  
Takahiro Katsuki ◽  
Yasuhiro Yoda ◽  
Tatsuya Masuda ◽  
...  
Keyword(s):  
Glucose Intolerance ◽  
High Fat Diet ◽  
Cell Function ◽  
Cell Mass ◽  
Male Rats ◽  
Standard Diet ◽  
Pancreatic Β Cell ◽  
Β Cells ◽  
Β Cell ◽  
Β Cell Function

We previously demonstrated that androgen signaling expands pancreatic β-cell mass in the sexual maturation period ( Am J Physiol Endocrinol Metab 314: E274–E286, 2018). The aim of this study was to elucidate whether fetal androgen signaling plays important roles in β-cell mass development and β-cell function in adulthood, defects of which are associated with type 2 diabetes mellitus. In the pancreas of male fetuses, androgen receptor (AR) was strongly expressed in the cytoplasm and at the cell membrane of Nkx6.1-positive β-cell precursor cells but was markedly reduced in insulin-positive β-cells. Administration of the anti-androgen flutamide to pregnant dams during late gestation reduced β-cell mass and Ki67-positive proliferating β-cells at birth in a male-specific manner without affecting body weight. The decrease of β-cell mass in flutamide-exposed male rats was not recovered when rats were fed a standard diet, whereas it was fully recovered when rats were fed a high-fat diet (HFD), at 6 and 12 wk of age. Flutamide exposure in utero led to the development of glucose intolerance in male rats due to a decrease in insulin secretion when fed HFD but not standard diet. Insulin sensitivity did not differ between the two groups irrespective of diet. These results indicated that the action of fetal androgen contributed to β-cell mass expansion in a sex-specific manner at birth and to the development of glucose intolerance by decreasing the secretion of insulin in HFD-fed male rats. Our data demonstrated the involvement of fetal androgen signaling in hypothesized sex differences in the developmental origins of health and disease by affecting pancreatic β-cell function.

scholarly journals Bacteroides Uniformis CECT 7771 Alleviates Inflammation Within the Gut-adipose Tissue Axis, Involving TLR5 Signaling, in Diet-Induced Obese Mice

2021 ◽  
Author(s):  
Emanuel Fabersani ◽  
Kevin Portune ◽  
Isabel Campillo ◽  
Inmaculada López-Almela ◽  
Sergio Montserrat-de la Paz ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Body Weight Gain ◽  
Western Diet ◽  
Lymphoid Cells ◽  
Epididymal Adipose Tissue ◽  
Oral Glucose ◽  
Standard Diet ◽  
Intestinal Bacterium ◽  
Metabolic Dysfunction ◽  
Obese Mice

Abstract This study investigated the immune mechanisms whereby administration of Bacteroides uniformis CECT 7771 reduces metabolic dysfunction in obesity. C57BL/6 adult male mice were fed a standard diet or a Western diet high in fat and fructose, supplemented or not with B. uniformis CECT 7771 for 14 weeks. B. uniformis CECT 7771 reduced body weight gain, plasma cholesterol, triglyceride, glucose, and leptin levels; and improved oral glucose tolerance in obese mice. Moreover, B. uniformis CECT 7771 modulated the gut microbiota and immune alterations associated with obesity, increasing Tregs and reducing B cells, total macrophages and the M1/M2 ratio in both the gut and epididymal adipose tissue (EAT) of obese mice. B. uniformis CECT 7771 also increased the concentration of the anti-inflammatory cytokine IL-10 in the gut, EAT and peripheral blood, and protective cytokines TSLP and IL-33, involved in Treg induction and type 2 innate lymphoid cells activation, in the EAT. It also restored the obesity–reduced TLR5 expression in the ileum and EAT. The findings indicate that the administration of a human intestinal bacterium with immunoregulatory properties on the intestinal mucosa helps reverse the immuno-metabolic dysfunction caused by a Western diet acting over the gut-adipose tissue axis.

Mesotheliomas and Proliferative Lesions of the Testicular Mesothelium Produced in Fischer, Sprague-Dawley and Buffalo Rats by Methyl(acetoxymethyl)nitrosamine (DMN-OAc)

1979 ◽  
Vol 16 (5) ◽  
pp. 574-582 ◽  
Author(s):  
J. J. Berman ◽  
J. M. Rice
Keyword(s):  
Body Weight ◽  
Tumor Cells ◽  
Mesothelial Cells ◽  
Male Rats ◽  
Sprague Dawley ◽  
Colloidal Iron ◽  
Microscopic Appearance ◽  
Intraperitoneal Dose ◽  
Single Focus

A single intraperitoneal dose of methyl(acetoxymethyl)nitrosamine (13 mg/kg body weight) given to 78 5-week-old male rats induced 25 mesotheliomas; two mesotheliomas were found in 67 control rats. All mesotheliomas arose from the peritesticular mesothelium and had a typical microscopic appearance of branching papillary fronds with a collagenous core covered by one or many layers of plump tumor cells. Cytoplasm of tumor cells contained material that reacted positively to a colloidal iron stain and was labile to hyaluronidase. In addition to frank mesotheliomas, 16 lesions, which we called atypical mesothelial proliferations. were found. These consisted of a single focus of plump mesothelial cells overlying an area of thick stroma. Often these foci included short, non-branched papillary projections above the surface of adjacent normal mesothelium. Twelve of the 16 lesions occurred in methyl(acetoxymethyl)nitrosamine-treated rats.

scholarly journals Neonatal nutritional programming impairs adiponectin effects on energy homeostasis in adult life of male rats

2018 ◽  
Vol 315 (1) ◽  
pp. E29-E37 ◽  
Author(s):  
Mariana Peduti Halah ◽  
Paula Beatriz Marangon ◽  
Jose Antunes-Rodrigues ◽  
Lucila L. K. Elias
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Food Intake ◽  
White Adipose Tissue ◽  
Energy Homeostasis ◽  
Body Weight Gain ◽  
Adult Life ◽  
Male Rats ◽  
Nutritional Programming

Neonatal nutritional changes induce long-lasting effects on energy homeostasis. Adiponectin influences food intake and body weight. The aim of this study was to investigate the effects of neonatal nutritional programming on the central stimulation of adiponectin. Male Wistar rats were divided on postnatal (PN) day 3 in litters of 3 (small litter, SL), 10 (normal litter, NL), or 16 pups/dam (large litter, LL). We assessed body weight gain for 60 days, adiponectin concentration, and white adipose tissue weight. We examined the response of SL, NL, and LL rats on body weight gain, food intake, oxygen consumption (V̇o2), respiratory exchange ratio (RER), calorimetry, locomotor activity, phosphorylated-AMP-activated protein kinase (AMPK) expression in the hypothalamus, and uncoupling protein (UCP)-1 in the brown adipose tissue after central stimulus with adiponectin. After weaning, SL rats maintained higher body weight gain despite similar food intake compared with NL rats. LL rats showed lower body weight at weaning, with a catch up afterward and higher food intake. Both LL and SL groups had decreased plasma concentrations of adiponectin at PN60. SL rats had increased white adipose tissue. Central injection of adiponectin decreased body weight and food intake and increased V̇o2, RER, calorimetry, p-AMPK and UCP- 1 expression in NL rats, but it had no effect on SL and LL rats, compared with the respective vehicle groups. In conclusion, neonatal under- and overfeeding induced an increase in body weight gain in juvenile and early adult life. Unresponsiveness to central effects of adiponectin contributes to the imbalance of the energy homeostasis in adult life induced by neonatal nutritional programming.

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