Mass In Rats Research Articles

Inherent control of hepatocyte proliferation after subtotal liver resection.

At the normal physiological conditions, hepatocytes predominantly reside in G0 phase of cell cycle; they actively proceed to G1 phase upon damage to the organ. As it was shown in experiments with restoration of liver mass in rats after subtotal hepatectomy (resection of 80% of the organ mass may be considered as a model of the 'small for size' liver syndrome), the growth inhibition is due to prolonged arrest of hepatocyte proliferation, molecular mechanisms of which remain understudied. In a rat model of liver regeneration after surgical removal of 80% of its mass, we observe a delayed onset of hepatocyte proliferation: Ki67+ hepatocytes begin to appear as late as at 30 h after liver subtotal resection. Their appearance coincides with the beginning of transcription of genes for cyclins A2, B1, D 1 , and E 1 at 24-30 h after surgery. The corresponding increase in concentrations of cyclin D 1 and E proteins is further delayed till 48 h after liver resection. We have also observed a prolonged decrease in the expression of proto-oncogene c-met (the hepatocyte growth factor receptor-encoding gene Met), an increase in expression of the transforming growth factor β1 (TGFβ 1 ) receptor-encoding gene Tgfbr2. At the same time, irreversible block of hepatocyte proliferation is prevented by expression of certain factors, notably of the TWEAK/Fn14 signaling pathway: concentrations of the corresponding proteins in remnant livers have peaked from 24 to 48 h after liver subtotal resection.

Effects of simulated high-altitude hypobaric hypoxia on cardiac structure and function in rats

To investigate the effects of simulated hypobaric hypoxia environment at 7 000 m above sea level on cardiac structure and function in rats. A total of 96 male SD rats were randomly divided into high-altitude hypobaric hypoxia group (hypoxia group) and normobaric normoxia group (control group). Rats of hypoxia group were placed in a large cabin simulated 7 000 m high-altitude hypobaric hypoxia environment. Operating time 23 h / d, the control circadian ratio of approximately 12 h:12 h. The rats in control group were bred under normobaric normoxia. The hypoxic group was divided into 3 d, 7 d, 14 d, 28 d groups according to hypoxic time, 12 rats in each group. Changes of structure and function of heart due to hypoxia were evaluated by echocardiography and electrocardiogram. Myocardial pathological changes were analyzed by hematoxylin-eosin staining(HE). Compared with the control group at the same time point ①With prolonged exposure to hypobaric hypoxia, the growth ratio of body mass in rats is slower. Arterial oxygen saturation was significantly lower in both 14 d and 28 d (P＜0.05). ② Left ventricular end-diastolic anterior wall thickness (LVAWD) and left ventricular end-diastolic posterior wall thickness (LVPWD) of rats in 28 d were increased significantly (P＜0.05). Left ventricular end-diastolic diameter (LVIDD) and left ventricular internal dimension systole (LVIDS) of rats in 28 d were decreased significantly (P＜0.05, P＜0.01). Left ventricular ejection fraction (EF), fractional shortening of left ventricle (FS), pulmonary vein (PV) peak velocity and PV peak gradient of rats in 7 d were decreased significantly (P＜0.05, P＜0.01). ③The QRS and QT interval period were significantly prolonged in 14 d and 28 d (P＜0.05, P＜0.01). The ST was significantly lower in 3 d and 7 d (P＜0.05, P＜0.01). The amplitude of R wave gradually shifted downward in 7 d, 14 d, 28 d (P＜0.05, P＜0.01). ④The red blood cell (RBC), hemoglobin (HGB), red blood cell distribution width (RDW) in hypoxic group were increased significantly (P＜0.01). The platelet count (PLT) count was decreased significantly in 14 d and 28 d (P＜0.01). The serum creatinine (CR) was increased significantly in 14 d and 28 d (P＜0.05). ⑤Pathological changes such as myocardial edema, sarcolemma condensate, focal degeneration and necrosis with inflammatory cell infiltration could be found at early stage of hypoxia. Myocardial compensatory repair such as myocardial fibroblasts proliferation was significant at end stage of hypoxia. Left ventricular systolic functions of rats were decreased significantly after exposure to high altitude hypoxia hypobaric. The left ventricular systolic functions would recovery compensatory after one week exposed to high altitude hypoxia hypobaric.

CHANGES IN THE COLLAGEN CONTENT IN THE DERMIS OF RATS AFTER LOCAL COLD INJURIES

Changes in collagen mass in rats were studied under the conditions of local cold injuries. A method for quantitative determination of collagen in the dermis was developed and applied for the first time. Cold injury was replicated in mongrel male and female rats weighing 180–200 grams by applying a metal weight 2.5 cm in diameter, cooled in liquid nitrogen, to depilated skin on the back. A statistically significant decrease in collagen content was recorded in rats on day 3 after cold damage. Starting with the 14 th day after the cold injury, an increase in collagen content was observed due to the restored activity of fibroblasts. By the 21 st day, collagen content continued increasing, but full recovery was not observed.

Changes in the reactivity of vessels of rats with an experimental decrease in the mass of functioning nephrons

The aim : to evaluate changes in endothelium-dependent regulation of the tone of blood vessels (aorta and superior mesenteric artery) in rats 4 months after the removal of 5/6 renal tissue. Material and methods. An experimental CKD model was created by resection of 5/6 mass of renal tissue. The experimental group included animals (n = 12), subjected to nephrectomy (NE). The control group consisted of sham-operated (SO) rats (n = 10). Researches of vascular reactivity were performed on ring segments 2 mm long, which were excised from the aorta and superior mesenteric artery (SMA). A total of 23 segments of the aorta and 17 segments of SMA from rats after NE and 18 segments of the aorta and 15 segments of SMA from control animals were prepared. To measure the strength of contractions of the drugs, a FORT-10 sensor (WPI, USA) was used. The effects of acetylcholine (Ach, 1 x10 -6 M) on blood vessels, previously exposed to phenylephrine (1 x10 -5 M), and the response of vessels to Ach under conditions of prior exposure to TEA (1 x 10 -3 mol / l) and L-NAME (1 x10 -4 mol / l) were evaluated. Results. NE for a period of 4 months led to arterial hypertension - BP in the NE group of rats was higher (165, 0 ± 9.8 mm Hg) compared with SO (127.2 ± 9.7 mm Hg, р <0,001), and to myocardial remodeling (LVMI in NE rat was 2.72 ± 0.11 mg / g compared to 2.35 ± 0.09 mg / in the SO group, р <0,001 ). NE led to a decrease in dilatation of aortic and BWA fragments on the ACh compared with LO animals. Under the conditions of NO blocking, the NO synthase inhibitor — L-NAME — also had a lower response to ACh in rats with NE. The preliminary blockade of the Ca2 + -activated K + channels of high conductivity with the introduction of TEA resulted in a decrease in vasodilation caused by ACh in NE rat compared with the SO group. Conclusion. Resection of 5/6 of the kidney tissue mass in rats causes a decrease in vascular reactivity on the ACh. Endothelial dysfunction of rats after NE is associated with impairment of both NO-related and hyperpolarization-dependent endothelial cells in pathways of the vascular tone regulation.

A Novel Micronutrient Supplement to Mitigate the Transgenerational Effects of Paternal Obesity on Body Composition of Male Offspring (P11-138-19)

ObjectivesEmerging evidence suggests that paternal obesity plays a significant role on offspring health. Our previous work in rodents showed that high fat diet (HFD) induced paternal obesity reduced offspring glucose tolerance. It has also been reported that paternal obesity can initiate metabolic disturbance in subsequent generations. Therefore, we designed a novel micronutrient supplement to ameliorate the transgenerational effects of paternal obesity. MethodsFounder (F0) male Sprague Dawley rats (3 weeks, 12 per group) were weaned on control (CD) or HFD or diets containing micronutrient supplement (CS; HS), after which they were mated with CD fed females at 19 weeks of age. Twelve F1 offspring from each litter across the four diet groups were weaned on day 21 onto CD, generating four F1 groups. After 14 weeks on CD, they were mated with CD fed females. Male F2 siblings were fed CD or HFD from day 21. After 6 weeks on diet, they underwent EchoMRI (See attached study design). ResultsHFD increased adiposity (CD: 12.3%, HFD: 18.6%) in F0 which was normalized by supplementation (HS: 11.7%). Though no paternal effect on adiposity was found in F1 males across the four groups, supplementing F0 had significant impact on F2 body composition (fat mass, fat and lean percentage) without influencing body weight and lean mass after 6 weeks on diet.In F2, post weaning HFD significantly increased fat mass in rats from CD and HFD fed founders (CH vs CC P = 0.0001; HH vs HC P = 0.009) but this effect was significantly reduced by F0 supplementation irrespective of F0 diets (CSH vs CH P = 0.017; and HSH vs HH P = 0.04) [3-way ANOVA][See attached table].Moreover, lean percentage was decreased by post weaning HFD in rats from both non-supplemented F0 diet groups but interestingly this effect was significantly reduced only in rats sired by supplemented CD fed F0 (CSH > CH; P = 0.04). ConclusionsSupplementing CD fed grandfathers ameliorated the deleterious effect of HFD, decreasing fat deposition and increasing lean percentage whereas supplementing HFD fed F0 reduced only fat deposition without affecting lean mass of male grand offspring. Therefore, our designed supplement could eventually reduce the transgenerational effect of paternal obesity. Funding SourcesSupported by Australian NHMRC grant to MJM and CAM; MMB is supported by Scientia PhD Scholarship, UNSW. Supporting Tables, Images and/or Graphs▪▪

Wnt Signaling Mediated Inhibition of Osteoclastogenesis by Dietary Phenolic Hippuric Acid and 3-(3-hydroxyphenyl) Propionic Acid (3–3-PPA) (P01-037-19)

ObjectivesNutritional factors influence bone development. We have previously reported that Blueberry (BB) and BB-associated phenolic acids had significant effects on increasing bone mass in rats. We also found BB-associated phenolic acids [hippuric acid (HA) and 3-(3-hydroxyphenyl) propionic acid (3-3-PPA)] inhibited osteoclastogenesis in vitro and in ex vivo. Here, we investigated the mechanisms by which HA or 3-3-PPA inhibit osteoclast formation and if HA or 3-3-PPA inhibits bone resorption in vivo. MethodsMurine osteoclast (macrophage) cell line, RAW 264.7 cells, and hematopoietic osteoclast progenitor cells (isolated from 4 weeks old C57BL6/J mice) were cultured. Cells were treated with HA or 3-3-PPA (0.6, 6, 60, 600 μg/dL) for 4 days in the presence of 50 ng/ml of RANKL (Receptor activator of nuclear factor kappa-Β ligand). In animal studies, dietary HA or 3-3-PPA was provided at 1, 5 or 10 mg/kg/d to female mice for 4 weeks, starting at postnatal day 28. ResultsIn RAW 264.7 cell and primary cell cultures, TRAPase staining showed that RANKL-stimulated osteoclast number/well dose-dependently decreased with treatments of HA or 3-3-PPA. HA and 3-3-PPA significantly inhibited RANKL-induced β-catenin and GPR109A (G protein coupled receptor 109A) protein expression. Moreover, RANKL-induced β-catenin and GPR109A mRNA expression were also suppressed by HA and 3-3-PPA. Furthermore, after pre-treatment with HA or 3-3-PPA, RANKL-stimulated increases of Wnt/β-catenin down-stream genes such as c-myc, and osteoclastogenic genes such as NFkB and NFATc1 gene expression were blunted. In mice, we found significantly increased bone mass in dietary HA and 3-3-PPA supplemented groups compared to control group (P < 0.05). Increased bone mass in HA and 3-3-PPA treated mice was accompanied by decreased bone resorption (bone resorption markers and osteoclastogenic gene expression), but increased β-catenin expression in total protein isolated from bone. ConclusionsThese results indicate significant inhibition of osteoclastogenesis and bone resorption by HA and 3-3-PPA, and suggest that HA and 3-3-PPA inhibit bone marrow the hematopoietic cell differentiation program through non-canonical Wnt signaling to protect against increased bone resorption. Funding SourcesUSDA-ARS Project.

3,5 Diiodo-l-Thyronine (T₂) Promotes the Browning of White Adipose Tissue in High-Fat Diet-Induced Overweight Male Rats Housed at Thermoneutrality.

The conversion of white adipose cells into beige adipose cells is known as browning, a process affecting energy metabolism. It has been shown that 3,5 diiodo-l-thyronine (T2), an endogenous metabolite of thyroid hormones, stimulates energy expenditure and a reduction in fat mass. In light of the above, the purpose of this study was to test whether in an animal model of fat accumulation, T2 has the potential to activate a browning process and to explore the underlying mechanism. Three groups of rats were used: (i) receiving a standard diet for 14 weeks; (ii) receiving a high-fat diet (HFD) for 14 weeks; and (iii) receiving a high fat diet for 10 weeks and being subsequently treated for four weeks with an HFD together with the administration of T2. We showed that T2 was able to induce a browning in the white adipose tissue of T2-treated rats. We also showed that some miRNA (miR133a and miR196a) and MAP kinase 6 were involved in this process. These results indicate that, among others, the browning may be another cellular/molecular mechanism by which T2 exerts its beneficial effects of contrast to overweight and of reduction of fat mass in rats subjected to HFD.

Sinusoidal Electromagnetic Fields Increase Peak Bone Mass in Rats by Activating Wnt10b/β-Catenin in Primary Cilia of Osteoblasts

Extremely low-frequency electromagnetic fields have been considered a potential candidate for the prevention and treatment of osteoporosis; however, their action mechanism and optimal magnetic flux density (intensity) parameter are still elusive. The present study found that 50-Hz sinusoidal electromagnetic fields (SEMFs) at 1.8 mT increased the peak bone mass of young rats by increasing bone formation. Gene array expression studies with femoral bone samples showed that SEMFs increased the expression levels of collagen-1α1 and Wnt10b, a critical ligand of the osteogenic Wnt/β-catenin pathway. Consistently, SEMFs promoted osteogenic differentiation and maturation of rat calvarial osteoblasts (ROBs) in vitro through activating the Wnt10b/β-catenin pathway. This osteogenesis-promoting effect of SEMFs via Wnt10b/β-catenin signaling was found to depend on the functional integrity of primary cilia in osteoblasts. When the primary cilia were abrogated by small interfering RNA (siRNA) targeting IFT88, the ability of SEMFs to promote the osteogenic differentiation of ROBs through activating Wnt10b/β-catenin signaling was blocked. Although the knockdown of Wnt10b expression with RNA interference had no effect on primary cilia, it significantly suppressed the promoting effect of SEMFs on osteoblastic differentiation/maturation. Wnt10b was normally localized at the bases of primary cilia, but it disappeared (or was released) from the cilia upon SEMF treatment. Interestingly, primary cilia were elongated to different degrees by different intensities of 50-Hz SEMFs, with the window effect observed at 1.8 mT, and the expression level of Wnt10b increased in accord with the lengths of primary cilia. These results indicate that 50-Hz 1.8-mT SEMFs increase the peak bone mass of growing rats by promoting osteogenic differentiation/maturation of osteoblasts, which is mediated, at least in part, by Wnt10b at the primary cilia and the subsequent activation of Wnt/β-catenin signaling. © 2019 American Society for Bone and Mineral Research.

Investigation of the Lipid Changes That Occur in Hypertrophic Muscle due to Fish Protein-feeding Using Mass Spectrometry Imaging.

Alaska pollack protein (APP) was previously shown to reduce serum triacylglycerol and the atherogenic index and significantly increase gastrocnemius muscle mass in rats. To determine which myofibers are involved in this observed hypertrophy, we stained the gastrocnemius muscle with fast and slow fiber-specific antibodies and measured the muscle fiber diameter. We observed muscle hypertrophy in both the fast and slow fibers of APP-fed rats. Although muscle hypertrophy leads to drastic lipid changes, the amount of lipids did not differ significantly between casein-fed and APP-fed rats. To determine the lipid changes at the molecular species level and their localization, we performed matrix-assisted laser desorption/ionization mass spectrometry imaging to visualize lipids in the gastrocnemius muscles. We determined that lipid molecules were significantly changed due to APP feeding. Thus, APP feeding changes muscle lipid metabolism, and these metabolic changes might be related to hypertrophy.

Oestradiol and leptin have separate but additive anorexigenic effects and differentially target fat mass in rats.

We recently showed that male rats exhibit lower hypophagia and body weight loss compared to female rats following central leptin delivery, suggesting a role for oestradiol in leptin responsiveness. Accordingly, we delivered Ob (leptin) or GFP (control) gene into the brain of male rats that were simultaneously treated with oestradiol or vehicle. In a reciprocal approach, we compared oestradiol-deficient (OVX) with intact females (sham) that received leptin or control vector. Changes in food intake), body weight and body composition were examined. In males, oestradiol and leptin resulted in lower cumulative food intake (15%) and endpoint body weight (5%), although rats receiving dual treatment (oestradiol-leptin) ate 28% less and weighed 22% less than vehicle-control. Changes in food intake were unique to each treatment, with a rapid decrease in vehicle-leptin followed by gradual renormalisation. By contrast, hypophagia in oestradiol-control was of lower amplitude and sporadic. Leptin selectively targeted fat mass and endpoint abdominal fat mass was 65%-80% lower compared to their respective control groups. In females, both leptin groups had lower body weight (endpoint values 20% lower than control groups) with the highest extent in sham animals (endpoint value was 28% less in sham-leptin than in sham-control). OVX rats rapidly started regaining their lost body weight reminiscent of the pattern in males. Leptin rapidly and robustly reduced fat mass with endpoint values 30%-35% less than control treated animals. It appears that leptin and oestradiol decreased food intake and body weight via different mechanisms, with the pattern of oestradiol-leptin being reminiscent of that observed in females and the pattern of OVX-leptin reminiscent of that observed in males. Oestrogen status did not influence initial fat mass loss by leptin. It can be concluded that oestradiol modulates the long-term response to central leptin overexpression, although its actions on energy homeostasis are additive and independent of those of leptin.

Can lychee reducing the adipose tissue mass in rats?

ABSTRACT Lychee fruit has been studied owing to the presence of several bioactive compounds that can contribute to weight loss in obese individuals. However, the anti-obese potential of the fruit has not been explored yet. The aim of this study was to investigate the effect of different parts of lychee in reducing the adipose tissue mass of cafeteria diet-fed rats. Phenolic compounds and scavenging capacities were quantified. The food intake, apparent digestibility, weight of the body and liver, body mass, Lee Index, and the mass of epididymal and visceral adipose tissues were evaluated. The results were estimated by Tukey’s Test at 5% probability. A higher amount of phenolic compounds and scavenging capacity were observed in the peel of lychee as compared to the other parts of the fruit. The hypercaloric diet with lychee flour resulted in a higher apparent digestibility. There was no difference between groups control (C), hypercaloric (H), hypercaloric with lychee flour - 50.00% peel and 50.00% seeds (H2F), and hypercaloric with lychee flour - 33.33% peel, 33.33% pulp and 33.34% seeds (H3F) with respect to body and liver weight, corporal mass, and Lee Index. The hypercaloric diet-fed group exhibited an increase in visceral and epididymal adipose tissue mass, whereas the group fed with hypercaloric diets and flour made from the peel and seed of lychee presented a lower visceral adipose tissue mass. In conclusion, the use of lychee flour was considered viable because it decreased visceral adipose tissue mass in rats.

Siglec-15-targeting therapy increases bone mass in rats without impairing skeletal growth.

The treatment of juvenile osteoporosis has not been established due to a lack of data regarding the efficacy and adverse effects of therapeutic agents. The possible adverse effects of the long-term use of antiresorptive therapies on skeletal growth in children is of particular concern. Sialic acid-binding immunoglobulin-like lectin 15 (Siglec-15) is an immunoreceptor that regulates osteoclast development and bone resorption, and its deficiency suppresses bone remodeling in the secondary spongiosa, but not in the primary spongiosa, due to a compensatory mechanism of osteoclastogenesis. This prompted us to develop an anti-Siglec-15 therapy for juvenile osteoporosis because most anti-resorptive drugs have potential adverse effects on skeletal growth. Using growing rats, we investigated the effects of an anti-Siglec-15 neutralizing antibody (Ab) on systemic bone metabolism and skeletal growth, comparing this drug to bisphosphonate, a first-line treatment for osteoporosis. Male 6-week-old F344/Jcl rats were randomized into six groups: control (PBS twice per week), anti-Siglec-15 Ab (0.25, 1, or 4 mg/kg every 3 weeks), and alendronate (ALN) (0.028 or 0.14 mg/kg twice per week). Treatment commenced at 6 weeks of age and continued for the next 6 weeks. Changes in bone mass, bone metabolism, bone strength, and skeletal growth during treatment were analyzed. Both anti-Siglec-15 therapy and ALN increased bone mass and the mechanical strength of both the femora and lumbar spines in a dose-dependent manner. Anti-Siglec-15 therapy did not have a significant effect on skeletal growth as evidenced by micro-CT-based measurements of femoral length and histology, whereas high-dose ALN resulted in growth retardation with histological abnormalities in the growth plates of femurs. This unique property of the anti-Siglec-15 Ab can probably be attributed to compensatory signaling for Siglec-15 inhibition in the primary spongiosa, but not in the secondary spongiosa. Thus, anti-Siglec-15 therapy could be a safe and effective for juvenile osteoporosis.

Osteoglycin post-transcriptional regulation by miR-155 induces cellular architecture changes in H9c2 cardiomyoblasts

Several studies have demonstrated dysregulated cardiac microRNAs (miRNAs) following cardiac stress and development of cardiac hypertrophy and failure. miRNAs are also differentially expressed in the inflammation that occurs in heart failure and, among these inflammatory-related miRNAs, the miR-155 has been implicated in the regulation of cardiac hypertrophy. Despite these data showing the role of miRNA-155 in cardiomyocyte hypertrophy under a hypertrophic stimulus, it is also important to understand the endogenous regulation of this miRNA without a hypertrophic stimulus to fully appreciate its function in this cell type. The first aim of the present study was to determine whether, without a hypertrophic stimulus, miR-155 overexpression induces H9c2 cardiac cells hypertrophy in vitro. The second objective was to determine whether osteoglycin (Ogn), a key regulator of heart mass in rats, mice, and humans, is post-transcriptionally regulated by miR-155 with a potential role in inducing H9c2 cells hypertrophy. Here, we show that, without a hypertrophic stimulus, miR-155 significantly repressed Ogn protein levels, but induce neither alteration in morphological phenotype nor in the expression of the molecular markers that fully characterize pathological hypertrophy of H9c2 cells. However, most importantly, Ogn silencing in H9c2 cells mimicked the effects of miR-155 overexpression in inducing cellular architecture changes that were characterized by a transition of the cell shape from fusiform to rounded. This is a new role of the post-transcriptional regulation of Ogn by miR-155 in the maintenance of the cardiac cell morphology in physiological and pathological conditions.

Intensity‑dependent effect of treadmill running on differentiation of rat bone marrow stromal cells.

The effect of running on bone mass depends on its intensity. However, the underlying molecular mechanism that associates running intensity with bone mass is unclear. The current study examined the effects of treadmill running at different intensities on bone mass and osteogenic differentiation of bone marrow stromal cells (BMSCs) in a rat model. A total of 24 male Wistar rats were randomly divided into groups and subjected to no running (Con group), low-intensity running (LIR group), moderate-intensity running (MIR group), and high-intensity running (HIR group). Histological, immunohistochemistry and micro-CT examinations were performed on the femora harvested after 8 weeks of treadmill running. The study demonstrated that treadmill running affected trabecular bone mass in an intensity-dependent manner. In addition, such an intensity-dependent effect was also demonstrated on the osteogenic and adipogenic differentiation and proliferation of BMSCs. Furthermore, the Wnt/β-catenin signaling pathway may be involved in the running-induced increase in bone mass in rats in the MIR group. There appears to be a biomechanical ‘window’, in which running-induced strain signals can increase the number of BMSCs and progenitor cells (specific to the osteoblast lineage) causing upregulation of osteogenesis and downregulation of adipogenesis of BMSCs. This finding may provide insight into the molecular and cellular mechanisms responsible for bone homeostasis.

Mesenchymal Stem Cells Reduce Left Ventricular Mass in Rats with Doxorubicin-Induced Cardiomyopathy

Mesenchymal Stem Cells Reduce Left Ventricular Mass in Rats with Doxorubicin-Induced Cardiomyopathy

Hepatic GIP expression is modified by supplementing high-dose thiamine in obese diabetic rats

Obesity is linked with type 2 diabetes in terms of increasing the risk of developing type 2 diabetes and that of its associated morbidity. We previously reported that thiamine supplementation decreases body weight and visceral fat mass in rats with obesity-related diabetes. Glucose-dependent insulinotropic polypeptide (GIP) acts on pancreatic β cells to promote insulin secretion. According to established theory, GIP is derived from the gastrointestinal tract. We previously discovered increased expression of the incretin GIP gene (Gip) in the livers of obese rats with diabetes receiving high-dose thiamine. We focused on liver-derived GIP to demonstrate GIP protein expression in the liver and visually present localization of GIP in the liver.

Fructo-oligosaccharides reduce energy intake but do not affect adiposity in rats fed a low-fat diet but increase energy intake and reduce fat mass in rats fed a high-fat diet

The ingestion of low or high lipid diets enriched with fructo-oligosaccharide (FOS) affects energy homeostasis. Ingesting protein diets also induces a depression of energy intake and decreases body weight. The goal of this study was to investigate the ability of FOS, combined or not with a high level of protein (P), to affect energy intake and body composition when included in diets containing different levels of lipids (L). We performed two studies of similar design over a period of 5weeks. During the first experiment (exp1), after a 3-week period of adaptation to a normal protein-low fat diet, the rats received one of the following four diets for 5weeks (6 rats per group): (i) normal protein (14% P/E (Energy) low fat (10% L/E) diet, (ii) normal protein, low fat diet supplemented with 10% FOS, (iii) high protein (55%P/E) low fat diet, and (iv) high protein, low fat diet supplemented with 10% FOS. In a second experiment (exp2) after the 3-week period of adaptation to a normal protein-high fat diet, the rats received one of the following 4 diets for 5weeks (6 rats per group): (i) normal protein, high fat diet (35% of fat), (ii) normal protein, high fat diet supplemented with 10% FOS, (iii) high protein high fat diet and (iv) high protein high fat diet supplemented with 10% FOS. In low-fat fed rats, FOS did not affect lean body mass (LBM) and fat mass but the protein level reduced fat mass and tended to reduce adiposity. In high-fat fed rats, FOS did not affect LBM but reduced fat mass and adiposity. No additive or antagonistic effects between FOS and the protein level were observed. FOS reduced energy intake in low-fat fed rats, did not affect energy intake in normal-protein high-fat fed rats but surprisingly, and significantly, increased energy intake in high-protein high-fat fed rats. The results thus showed that FOS added to a high-fat diet reduced body fat and body adiposity.

Dietary egg-white protein increases body protein mass and reduces body fat mass through an acceleration of hepatic β-oxidation in rats.

Egg-white protein (EWP) is known to reduce lymphatic TAG transport in rats. In this study, we investigated the effects of dietary EWP on body fat mass. Male rats, 4 weeks old, were fed diets containing either 20 % EWP or casein for 28 d. Carcass protein levels and gastrocnemius leg muscle weights in the EWP group were significantly higher than those in the casein group. In addition, carcass TAG levels and abdominal fat weights in the EWP group were significantly lower than those in the casein group; adipocyte size in abdominal fat in the EWP group was smaller than that in the casein group. To identify the involvement of dietary fat levels in the rats, one of two fat levels (5 or 10 %) was added to their diet along with the different protein sources (EWP and casein). Abdominal fat weight and serum and hepatic TAG levels were significantly lower in the EWP group than in the casein group. Moreover, significantly higher values of enzymatic activity related to β-oxidation in the liver were observed in the EWP group compared with the casein group. Finally, abdominal fat weight reduction in the EWP group with the 10 % fat diet was lower than that in the EWP group with the 5 % fat diet. In conclusion, our results indicate that, in addition to the inhibition of dietary TAG absorption reported previously, dietary EWP reduces body fat mass in rats through an increase of body protein mass and the acceleration of β-oxidation in the liver.

Effects of flour or flaxseed oil upon testis mass in rats subjected to early weaning

Study evaluates testis mass in rats subjected to early weaning and subsequently nourished with diet containing flour or flaxseed oil. Pups were weaned for separation from mothers at 14 days (early weaning, EW) and 21 days (control, C). After 21 days, the control group (C60) was nourished with control diet. EW was divided as: control (EWC60), flaxseed flour (EWFF60) and flaxseed oil (EWFO60) group diets for the next 60 days. At 21st and 60th day, body mass, serum cholesterol and triglycerides and testis mass were evaluated. At 21 day, EW group showed lower (p < 0.05) body mass, serum cholesterol and testis mass. At 60 days, EWC60 and EWFO60 groups showed lower (p < 0.05) body mass (vs. C60 and EWFF60). EWFF60 group showed lower (p < 0.05) serum cholesterol (vs. EWC60 and EWFO60) and higher (p < 0.05) testis mass (vs. C60, EWC60 and EWFO60). Flaxseed flour (vs. oil) was associated with higher testis mass following early weaning.

Isoflavin-β modifies muscle oxidative stress and prevents a thyrotoxicosis-induced loss of muscle mass in rats.

We sought to verify whether isoflavin-beta (Iso-β), a mixture of isoflavones with antioxidant properties, could prevent thyrotoxicosis-induced loss of muscle mass and the participation of oxidative stress (OS) in the mechanisms of this prevention. Two experimental periods of thyrotoxicosis induction were used in Wistar rats: 3 and 5 days to assess Iso-β effects before and after thyrotoxicosis-induced muscle wasting. After euthanasia, peritoneal fat and gastrocnemius muscle were collected, weighed, and muscle OS was assessed. Iso-β prevented the loss of gastrocnemius mass in thyrotoxic rats through the prevention of muscle OS generation during thyrotoxicosis, increasing muscle total antioxidant capacity and decreasing mitochondrial cytochrome c oxidase activity, lipid peroxidation, and protein carbonyl content. Iso-β decreased oxidative modification of proteins, which is known to exert a major role during proteolysis induction and is present in thyrotoxic myopathy, highlighting the potential action of Iso-β in this complication of the disease. Muscle Nerve 56: 975-981, 2017.