Homeostasis In Rats Research Articles

Leptin Receptors Are Not Required for Roux-en-Y Gastric Bypass Surgery to Normalize Energy and Glucose Homeostasis in Rats.

Sensitization to the adipokine leptin is a promising therapeutic strategy against obesity and its comorbidities and has been proposed to contribute to the lasting metabolic benefits of Roux-en-Y gastric bypass (RYGB) surgery. We formally tested this idea using Zucker fatty fa/fa rats as an established genetic model of obesity, glucose intolerance, and fatty liver due to leptin receptor deficiency. We show that the changes in body weight in these rats following RYGB largely overlaps with that of diet-induced obese Wistar rats with intact leptin receptors. Further, food intake and oral glucose tolerance were normalized in RYGB-treated Zucker fatty fa/fa rats to the levels of lean Zucker fatty fa/+ controls, in association with increased glucagon-like peptide 1 (GLP-1) and insulin release. In contrast, while fatty liver was also normalized in RYGB-treated Zucker fatty fa/fa rats, their circulating levels of the liver enzyme alanine aminotransferase (ALT) remained elevated at the level of obese Zucker fatty fa/fa controls. These findings suggest that the leptin system is not required for the normalization of energy and glucose homeostasis associated with RYGB, but that its potential contribution to the improvements in liver health postoperatively merits further investigation.

Hexagonal boron nitride nanoparticles trigger oxidative stress by modulating thiol/disulfide homeostasis.

Hexagonal boron nitride nanoparticles (hBN NPs) are encouraging nanomaterials with unique chemical properties in medicine and biomedical fields. Until now, the optimal hBN NP's dosage and biochemical mechanism that can be used for in vivo systems has not been fully revealed. The main aim of this article is to reveal characteristics, serum and tissue interactions and any acute cytotoxic effect of different dose of hBN NPs for the first time. hBN NPs at concentrations varying between 50-3200 µg/kg was administered by intravenous injection to Wistar albino rats (n = 80) divided into seven dosage and control groups. Blood and tissue samples were taken after 24 hours. Our findings suggested that higher doses hBN NPs caused oxidative stress on the serum of rats dose-dependently. However, hBN NPs did not affect thiol/disulfide homeostasis on kidney, liver, spleen, pancreas and heart tissue of rats. Furthermore, hBN NPs increased serum disulfide formation by disrupting the thiol/disulfide balance in rats. Also, LOOH and MPO levels increased at high doses, while CAT levels decreased statistically. The results revealed that hBN NPs induce oxidative stress in a dose-dependent manner by modulating thiol/disulfide homeostasis in rats at higher concentrations.

Olive oil and exercise training ameliorate muscle mitochondrial homeostasis in rats fed a high-fat diet

Olive oil and exercise training ameliorate muscle mitochondrial homeostasis in rats fed a high-fat diet

Hepatoprotective efficiency of selenolin studied on the model of acute liver failure in rats

The influence of selenolin on the metabolic functions of the liver of laboratory rats was studied on the model of the reproduction of acute liver failure caused by acetaminophen. It was determined that the use of selenolin inhibits and weakens the hepatotoxic effects, contributing to the correction of impaired homeostasis in rats. Under the action of the preparation, there was a decrease in enzymatic activity – AST – in 2.35 times, ALT – in 2.4 times, γ-GGT – by 21.7%, as well as an improvement in protein synthesizing function, manifested by an increase in the concentration of total protein by 26.9%. Selenolin significantly (p <0.05) reduces the level of lipid peroxidation products – DC – in 1.5 times, CD – by 56.3%, MDA – by 19.9%. Due to the organic selenium included in the preparation, selenolin helps to maintain a high activity of the enzyme antioxidant system, which leads to a decrease in the stationary level of free radical and lipid peroxidation products, allowing the body to quickly cope with pathological changes in the liver cells and in the blood homeostasis system.

Impact of combined long-term fructose and prednisolone intake on glucose and lipid homeostasis in rats: benefits of intake interruption or fish oil administration

We investigated whether combined long-term fructose and prednisolone intake would be more detrimental to the glucose homeostasis than if ingested separately. We also evaluated whether fish oil administration or interruption of treatments has any positive impact. For this, male adult Wistar rats ingested fructose (20%) (F) or prednisolone (12.5 µg/mL) (P) or both (FP) through drinking water for 12 weeks. A separate group of fructose and prednisolone-treated rats received fish oil treatment (1 g/kg) in the last 6 weeks. In another group, the treatment with fructose and prednisolone was interrupted after 12 weeks, and the animals were followed for more 12 weeks. Control groups ran in parallel (C). The F group had higher plasma TG (+42%) and visceral adiposity (+63%), whereas the P group had lower insulin sensitivity (−33%) and higher insulinemia (+200%). Only the the FP group developed these alterations combined with higher circulating uric acid (+126%), hepatic triacylglycerol content (+16.2-fold), lipid peroxidation (+173%) and lower catalase activity (−32%) that were associated with lower protein kinase B content and AMP-activated protein kinase (AMPK) phosphorylation in the liver, lower AMPK phosphorylation in the adipose tissue and higher beta-cell mass. Fish oil ingestion attenuated the elevation in circulating triacylglycerol and uric acid values, while the interruption of sugar and glucocorticoid intake reverted almost all modified parameters. In conclusion, long-term intake of fructose and prednisolone by male rats are more detrimental to glucose and lipid homeostasis than if ingested separately and the benefits of treatment interruption are broader than fish oil treatment.

"Live High Train Low" Hypoxic Training Enhances Exercise Performance with Efficient Redox Homeostasis in Rats' Soleus Muscle.

Çolak, Rıdvan, Eda Ağaşcıoğlu, and Ufuk Çakatay. "Live high train low" hypoxic training enhances exercise performance with efficient redox homeostasis in rats' soleus muscle. High Alt Med Biol. 22:77-86, 2021. Background: Different types of hypoxic training have been performed to improve exercise performance. Although both "live high train high" and "live high train low" techniques are commonly performed, it is still obscure as to which one is more beneficial. Materials and Methods: Eight-week-old male Sprague-Dawley rats were randomly divided into aforementioned experimental groups. After a familiarization exercise (4-week, ∼15-30 minutes/day) at normoxia, all rats exercised (4-week, ∼35 minutes/day) at hypoxia with their pre-evaluated maximal aerobic velocity test. The soleus was extracted after the test following 2 days of resting. Results: The live high trained low group displayed better performance than the live high trained high (p = 0.031) and the live low trained low (p = 0.017) groups. Redox status biomarkers were higher in the live high trained high group except for thiols, which were illustrated with no difference among the groups. Further, contrary to total and protein thiols (r = 0.57, p = 0.037; r = 0.55, p = 0.042 respectively), other redox status biomarkers were observed to be negatively correlated to exercise performance. Conclusions: The live high trained low group could consume more oxygen during exercise, which might lead to having a better chance to ensure cellular redox homeostasis. Therefore, this group could ensure an optimum exercise performance and anabolic metabolism.

Time restricted feeding provides a viable alternative to alternate day fasting when evaluated in terms of redox homeostasis in rats

Intermittent fasting (IF) is a non-pharmacological dietary approach for intervening into aging in different organisms. We evaluated the efficacy of time restricted dietary regimen and alternate-day fasting in rats by measuring redox parameters which are frequently used as signature biomarkers of aging. Wistar rats (8 months) were divided into three groups of six rats each. Group I: Control; Group II: Time-restricted feeding (TRF) (fed and fasted at a ratio of 16:8 h respectively) and Group III. Alternate day feeding (ADF) (fed and fasted on alternate days), for a period of 1 month. The biomarkers of antioxidant defense and oxidative stress: FRAP, GSH, PMRS, ROS, AGE, MDA, PCO, AOPP, TNF-α and IL-6, were determined. Our results suggest that, based on predominant aging biomarkers, TRF has a similar effect on rats compared with ADF evaluated in terms of redox homeostasis. Observed results defend our purpose that the ADF and TRF methods are reliable dietary restriction regimens and subsequently improve the metabolic profile and redox homeostasis in rats.

MO053INHIBITION OF SODIUM PHOSPHATE TRANSPORTER NPT2A IMPROVES EXPERIMENTAL VASCULAR CALCIFICATION AND PHOSPHATE HOMEOSTASIS IN RATS

Abstract Background and Aims A dysregulated phosphate homeostasis is strongly associated with mortality, cardiovascular events and vascular calcification, particularly in patients suffering from CKD. Inhibition of the tubular phosphate transporter Npt2a provides a novel and unique mechanism to address phosphate homeostasis imbalance and vascular calcification. Method Npt2a activity was measured in a cell-based assay, using a stable CHO cell line with inducible Npt2a expression. Male Wistar rats were used for all experiments. Healthy rats were treated orally with BAY 767, a potent Npt2a inhibitor developed at Bayer AG to assess urinary phosphate excretion. Vascular calcification was induced by administration of a pan-FGFR inh. (25mg/kg) for 10 days. Calcium content in the aorta was measured as surrogate for vascular calcification. Blood samples were withdrawn at the end of the study to determine the plasma levels of FGF-23, parathyroid hormone and phosphate with commercially available assay systems according to the manufactures protocols (FGF-23 and PTH: ELISA Kit, Immuntopics; phosphate: Pentra400 system). Results BAY 767 was identified as potent Npt2a inhibitor, with an IC50 of 2.9/6 nM on rat/ human Npt2a, respectively, selective over Npt2b, Npt2c and Pit-1. Single dose treatments of healthy rats resulted in a significant, dose-dependent increase in urinary phosphate excretion within 16h. In an experimental vascular calcification model, massive vascular calcification and hyperphosphatemia was induced by daily oral administration of a FGFR inh. Simultaneous treatment with the Npt2a inhibitor BAY 767 significantly inhibited vascular calcification in comparison to untreated rats. In this set-up the plasma phosphate level was increased after 10 days up to 3.7 mmol/L in the FGFR inh. treated group compared to 1.9 mmol/L in control animals, whilst treatment with BAY 767 reduced plasma levels to 2.7 mmol/L. In addition, FGF-23 and PTH were also reduced under compound BAY 767 treatment. However, in the same model 2.2% lanthanum carbonate was not beneficial with respect to vascular calcification. Conclusion Our results show for the first time that treatment with a Npt2a inhibitor improves vascular calcification by addressing urinary phosphate excretion and phosphate homeostasis in rats. Npt2a inhibition may provide a new therapeutic principle for patients suffering from disbalanced phosphate homeostasis and vascular calcifications, including CKD patients.

Early-adulthood caloric restriction is beneficial to improve renal redox status as future anti-aging strategy in rats

AimsCaloric restriction (CR) is an experimental approach proposed to alleviate age-related oxidative damage. In the present study, we investigated the consequences of CR on renal redox homeostasis in rats at a specific time frame in early-adulthood.. MethodsThree groups of male Sprague-Dawley rats; young control at 6-month-old, 2-year-old subjected to 40% CR between 18th-24th months of age, and their non-CR controls were sacrificed, and numerous redox status biomarkers including protein oxidation, glycation, lipid peroxidation, glycation end products, thiol groups, and superoxide dismutase were assayed. It was also ensured that CR rats and their non-CR corresponding rats had similar body weights at the end of the study to decrease the confounding effects of different body weights on redox homeostasis and caloric restriction. ResultsAfter CR, the detrimental effects of the protein oxidation, glycation, and lipid peroxidation were significantly improved in the renal tissue CR rats when compared to their non-CR control group. However, there were no significant difference in thiol fractions between younger controls and both of the elderly groups. ConclusionDetrimental consequences of renal senescence on redox homeostasis are significantly improved via CR especially applied in early-adulthood.

Effects of fullerene C60 supplementation on gut microbiota and glucose and lipid homeostasis in rats

The effects of twelve weeks of supplementation with fullerene C60 olive/coconut oil solution on a broad spectrum of parameters in rats were examined. The tissue bioaccumulation of C60 was shown to be tissue-specific, with the liver, heart, and adrenal glands being the organs of the greatest, and the kidney, brain, and spleen being the organs of the smallest accumulation. C60 did not change aspartate aminotransferase, alanine aminotransferase, and alkaline phosphatase serum activities level, nor the damage of liver cells DNA. There were no effects of fullerene on prooxidant-antioxidant balance in the liver, kidney, spleen, heart, and brain, nor any visible harmful effects on the liver, heart, aorta, spleen, kidney, and small intestine histology. Fullerene changed the gut microbiota structure towards the bacteria that ameliorate lipid homeostasis, causing a serum triglycerides concentration decrease. However, C60 significantly increased the insulin resistance, serum ascorbate oxidation, and brain malondialdehyde and advanced oxidation protein products level. The deteriorative effects of C60 on the brain and serum could be attributed to the specific physicochemical composition of these tissues, potentiating the C60 aggregation or biotransformation as the key element of its pro-oxidative action.

Relationship of Vitamin D-Deficient Diet and Irisin, and Their Impact on Energy Homeostasis in Rats.

Background and ObjectivePrevious studies have identified the role of irisin and vitamin D in energy homeostasis. However, the effect of irisin and vitamin D on energy regulation has not been thoroughly investigated. Therefore, in this study, the effects of a vitamin D-deficient diet and irisin on total energy expenditure (TEE), food intake, and blood metabolites were investigated in rats.MethodsSixteen healthy weaned male albino rats were randomly divided into two groups: a group fed a normal balanced growth diet (group A: n = 8) and a group fed a normocalcemic diet that is vitamin D deficient with limited ultraviolet (UV) light exposure (group B, n = 8). After 6 weeks, the volumes of respiratory gases were measured by open-circuit indirect calorimetry. Serum irisin, 25-OHVD3, calcium, insulin, and glucose levels were measured using ELISA. The respiratory quotient (RQ), energy expenditure, and Homeostatic Model Assessment for Insulin Resistance (HOMA-IR) were calculated.ResultsRats with hypovitaminosis D were hypoirisinemic. Food intake, RQ (to the range of using endogenous fat), and glucose levels reduced significantly, while insulin levels increased. Body weight and TEE were non-significant changed. Additionally, irisin was strongly and positively correlated with body weight under normal conditions (r = 0.905, p < 0.01), and a moderate negative correlation in group B (r = −0.429, p < 0.05). TEE and irisin showed no significant correlation.ConclusionThis study demonstrated that the early changes in energy homeostasis and irisin levels during states of hypovitaminosis D are affected by long-term consumption of a vitamin D-deficient diet with limited UV exposure.

Raspberry ketone attenuates high-fat diet-induced obesity by improving metabolic homeostasis in rats

Objective: To investigate the molecular mechanisms of the anti-obese effect of raspberry ketone against high-fat diet fed rats. Methods: Fifty adult male rats were randomly assigned to receive a standard diet, a high fat diet, and the high-fat diet and 0.5%, 1% or 2% raspberry ketone. Body weight, biochemical parameters and gene expression of CCAAT enhancer-binding protein (C/EBP)δ, fatty acid synthase (FAS), acetyl CoA carboxylase (ACC), peroxisome proliferator-activated receptor alpha (PPAR-α), hormone-sensitive lipase (HSL) and hepatic carnitine palmitoyltransferase 1 A (CPT1A) were investigated. Results: Body weight, blood glucose, insulin, total lipids, triacylglycerols, total cholesterol and low-density lipoprotein cholesterol were increased in high-fat diet fed rats. These high fat diet-induced changes were attenuated by treatment with raspberry ketone. High-density lipoprotein cholesterol was decreased in highfat diet fed rats but increased in rats treated with raspberry ketone. Molecular investigations showed induction of gene expression of C/EBP-δ, FAS, ACC, CPT1A and inhibition of gene expression of PPAR-α and HSL in high-fat diet fed rats as compared with control. Raspberry ketone treament reversed these changes except CPT1A. Conclusions: Raspberry ketone can prevent obesity induced by a high-fat diet in rats by induction of the expression of enzymes, controlling lipolysis and fatty acids β oxidation as well as inhibition of gene expressions of adipogenic factors.

Dose-Dependent Effects of Triclocarban Exposure on Lipid Homeostasis in Rats.

Environmental exposure to triclocarban (TCC), a common antibacterial agent widely used in thousands of personal care products, poses a potential risk for human health. Previous in vitro studies about biological effects of TCC have yielded a variety of inconsistent results and apparently not been verified in vivo. In the current study, dose-dependent effects of TCC exposure on lipid homeostasis in rats were investigated using a combination of untargeted 1H NMR metabolomics, targeted metabolite profiling (LC/GC-MS), histopathological assessments, and biological assays. Our results revealed that TCC dose-dependently activated aryl hydrocarbon receptor (AHR) and its transcriptional targets such as Cyp1a1 and Cyp1b1 in the liver of rats, suggesting that TCC may be a potent AHR agonist. Although TCC exhibited dose-dependent toxicity, oral exposure with relatively low dose TCC caused more significant hepatic lipogenesis of rats than relatively high and moderate doses of TCC. It was mainly manifested by histopathological observations and promotion of de novo fatty acid, phospholipid, and ceramide biosynthesis and gut microbiota fermentation. Our findings provide new insights into health effects of TCC exposure with different dosages in vivo, especially on the induction and progression of nonalcoholic fatty liver disease, and further our understanding in the pathogenesis of metabolic diseases induced by environmental pollutants.

Effect of a nanodispersion silica composite with polyhexamethylene guanidine hydrochloride on immunological indicators and indicators of oxidation and antioxidant homeostasis in rats with thermal burn

Worldwide, nearly 6 million people annually seek medical attention for burn wounds. Today, the main method of local treatment of wounds and burns, including infected ones, is the use of medicines containing antiseptics, antibiotics, sorbents, as well as their combinations.Purpose. To determine the effect of a nanosized silica composite with polyhexamethylene guanidine hydrochloride on the immunological parameters and oxidative-antioxidant homeostasis in the blood and in the lesion of rats with an uninfected thermal burn.Materials and methods. The study was conducted on 72 rats, which were modeled by a thermal burn of the II degree. The animals were divided into 4 groups: intact, control, treated with chlorhexidine, treated with a composite of nanosized silica with polyhexamethylene guanidine hydrochloride. On the 7th, 14th, 21st and 28th day, the animals were removed from the experiment and the immunological parameters and the parameters of oxidative-antioxidant homeostasis in the blood and skin in the lesion were determined.Results. Thermal injury is directly related to biochemical changes in the body. We compared the levels of anti- and pro-inflammatory cytokines, markers of free radical oxidation - diene conjugate (DC), the active products of thiobarbituric acid (TBA-AP), the activity of catalase (Cat) and superoxide dismutase (SOD). It was proved that the NDK + PHMG-GC composite showed significantly more pronounced compared with chlorhexidine, a pharmacological effect in reducing the level of pro-inflammatory cytokines IL-1β and TNF-α and an increase in the content of IL-10 in the blood and the focus of thermal burn during the entire observation period . Also, the composite effectively affects oxidation-antioxidant homeostasis, which is manifested in the normalization of the content of DC and TBA-AP on the 14th day, restoration of Cat activity on the 14th day, SOD - already on the 7th day compared with chlorhexidine.Conclusions. The study indicates that the NDS + PHMG composite has pronounced anti-inflammatory and wound healing properties, which allows it to be used as a combined preparation for the treatment of thermal burns

Maternal folic acid supplementation does not counteract the deleterious impact of prenatal exposure to environmental pollutants on lipid homeostasis in male rat descendants.

Prenatal exposure to persistent organic pollutants (POPs) has been associated with the development of metabolic syndrome-related diseases in offspring. According to epidemiological studies, father's transmission of environmental effects in addition to mother's can influence offspring health. Moreover, maternal prenatal dietary folic acid (FA) may beneficially impact offspring health. The objective is to investigate whether prenatal FA supplementation can overcome the deleterious effects of prenatal exposure to POPs on lipid homeostasis and inflammation in three generations of male rat descendants through the paternal lineage. Female Sprague-Dawley rats (F0) were exposed to a POPs mixture (or corn oil) +/- FA supplementation for 9 weeks before and during gestation. F1 and F2 males were mated with untreated females. Plasma and hepatic lipids were measured in F1, F2, and F3 males after 12-h fast. Gene expression of inflammatory cytokines was determined by qPCR in epididymal adipose tissue. In F1 males, prenatal POPs exposure increased plasma lipids at 14 weeks old and hepatic lipids at 28 weeks old and prenatal FA supplementation decreased plasma total cholesterol at 14 weeks old. Prenatal POPs exposure decreased plasma triglycerides at 14 weeks old in F2 males. No change was observed in inflammatory markers. Our results show an impact of the paternal lineage on lipid homeostasis in rats up to the F2 male generation. FA supplementation of the F0 diet, regardless of POPs exposure, lowered plasma cholesterol in F1 males but failed to attenuate the deleterious effects of prenatal POPs exposure on plasma and hepatic lipids in F1 males.

Joint and separate exposure to alcohol and \u22069-tetrahydrocannabinol produced distinct effects on glucose and insulin homeostasis in male rats

Cannabis and alcohol co-use is common, and the trend may increase further given the current popularity of cannabis legalization. However, the metabolic consequences of such co-use are unclear. Here, we investigated how co-administration of alcohol and ∆9-tetrahydrocannabinol (THC), the main psychoactive constituent of cannabis, affects body weight and visceral adiposity, and glucose and insulin homeostasis in rats. For 16 consecutive days during adolescence, male rats drank saccharin or alcohol after receiving subcutaneous oil or THC injections in Experiment 1 and voluntarily consumed alcohol, THC edible, or both drugs in Experiment 2. Experiment 1 showed that following abstinence, drug co-exposure reduced visceral fat and the amount of insulin required to clear glucose during an oral glucose tolerance test (OGTT). In Experiment 2, rats received a high-fat diet (HFD) after 3-week abstinence. Although adolescent drug use did not interact with the HFD to worsen hyperglycemia and hyperinsulinemia during an OGTT, HFD-fed rats that co-used alcohol and THC had the lowest insulin levels 75 min after an insulin injection, suggesting an altered rate of insulin secretion and degradation. These results suggest that THC and alcohol co-exposure can distinctly alter the physiology of glucose and insulin homeostasis in a rodent model.

Increased Body Weight and Fat Mass After Subchronic GIP Receptor Antagonist, but Not GLP-2 Receptor Antagonist, Administration in Rats.

Glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-2 (GLP-2) are hormones secreted from the enteroendocrine cells after a meal. They exert their actions through activation of G protein-coupled receptors (R), the GIPR and GLP-2R, respectively. Both have been reported to influence metabolism. The purpose of the study was to investigate the role of the hormones in the regulation of lipid and bone homeostasis by subchronic treatment with novel GIPR and GLP-2R antagonists. Rats were injected once daily with vehicle, GIPR, or GLP-2R antagonists for 3 weeks. Body weight, food intake, body composition, plasma lipoprotein lipase (LPL), adipokines, triglycerides and the marker of bone resorption carboxy-terminal collagen crosslinks (CTX), were examined. In rats, subchronic treatment with GIPR antagonist, rat GIP (3-30)NH2, did not modify food intake and bone resorption, but significantly increased body weight, body fat mass, triglycerides, LPL, and leptin levels compared with vehicle treated rats. Subchronic (Pro3)GIP (a partial GIPR agonist), GLP-2(11-33), and GLP-2(3-33) (GLP-2R antagonists) treatment did not affect any parameter. The present results would be consistent with a role for GIP, but not GLP-2, in the maintenance of lipid homeostasis in rats, while neither GIPR nor GLP-2R antagonism appeared to influence bone resorption in rats.

Modification Of Bile Acid Homeostasis By Iron Overload In Rats

Background and Aims: Excessive accumulation of iron (IO) in the liver accompany metabolic diseases associated with increased cholesterol plasma concentrations such as type II diabetes mellitus, metabolic syndrome, and nonalcoholic fatty liver disease (NAFLD). Bile acids (BA) are important endogenous metabolic regulators that modulate these pathologies but mutual relationship of IO and BA turnover is not thoroughly studied. The aim of present study was to describe effect of IO on BA homeostasis in rats.

Consumption of lycopene-rich tomatoes improved glucose homeostasis in rats via an increase in leptin levels.

The lycopene content of tomatoes is important because of its effects on vital physiological functions such as improvement of glucose tolerance and non-alcoholic fatty liver disease. To investigate the influence of the lycopene content of tomatoes on glucose tolerance and hepatic lipid content, homogenates of lycopene-rich (LR) or lycopene-free negative control (NC) tomato varieties were administrated to normal rats for 4weeks. At the end of the experiment, an oral glucose tolerance test (OGTT) was performed. Rats were fed once and then dissected. According to the OGTT results, plasma glucose levels in the LR group were 10% and 9% lower at 15min and 30min, respectively, than those in the NC group, whereas plasma insulin levels did not differ between the groups at either time point. Upon dissection, plasma leptin levels in the LR group were higher than those in the NC group, while plasma adiponectin levels did not differ between groups. With the exception of retinol palmitate, no carotenoids were detected in the liver by HPLC analysis. Hepatic retinol palmitate levels and hepatic triacyl glyceride levels did not differ between the groups. We concluded that in normal rats, a lycopene-rich tomato variety improved glucose tolerance via an increase in plasma leptin levels that enhanced insulin sensitivity but did not affect carotenoid accumulation or lipid metabolism.

Dietary gelatin enhances non-heme iron absorption possibly via regulation of systemic iron homeostasis in rats

Gelatin-based traditional Chinese medicines have long been used to treat anemia. Here, rats on the gelatin-based AIN-93G diet showed higher hemoglobin regeneration efficiencies and liver iron concentrations than those fed the diets based on several other animal proteins from muscle sarcoplasm and fibrils, egg white, whey and casein. However, among these animal proteins, gelatin had the lowest digestibility under simulated gastric-proximal intestinal digestion, and its hydrolysate showed the lowest capacity to aid iron absorption in Caco-2 monolayers via templating ferric oxyhydroxide nanoparticles. In another rat hemoglobin regeneration assay, dietary supplementations with gelatin and its two major degradation products, glycine and prolyl-hydroxyproline, revealed that gelatin boosted iron absorption not through glycine, but rather via prolyl-hydroxyproline, which had inhibitory and stimulatory effects on the plasma levels of hepcidin and erythropoietin, respectively. Dietary gelatin thus seems to enhance non-heme iron absorption via regulating systemic iron homeostasis rather than via solubilizing luminal ferric iron.