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This study investigated the anti-diabetic preventive activity of coenzyme Q sub(10) (CoQ sub(10)) in a murine model of diet-induced insulin resistance (IR), Psammomys obesus (Po). IR was induced by feeding a standard laboratory diet (SD). CoQ sub(10) oil suspension was orally administered at 10 mg/kg body weight (BW)/day along with SD for 9 months. Anthropometric parameters, namely, total body weight gain (BWG) and the relative weight of white adipose tissue (WAT) were determined. Blood glucose, insulin, quantitative insulin sensitivity check index (QUICKI), total antioxidant status (TAS), iron, malondialdehyde (MDA) and nitrite (NO sub(2) super(-)) were evaluated. NO sub(2) super(-) level was also assessed in peripheral blood mononuclear cells (PBMCs) culture supernatants. Our results show that CoQ sub(10) supplementation significantly improved blood glucose, insulin, QUICKI, TAS, iron and MDA, but influenced neither NO sub(2) super(-) levels nor the anthropometric parameters. These findings support the hypothesis that CoQ sub(10) would exert an anti-diabetic activity by improving both glycaemic control and antioxidant protection. The most marked effect of CoQ sub(10) observed in this study concerns the regulation of iron levels, which may carry significant preventive importance.

It has been previously shown that clinical cardiovascular manifestations can be caused by mild changes in thyroid function. However, the implication of angiotensinogen ( Agt ) and vascular smooth muscle cells (VSMCs) dysfunction in the pathophysiology of cardiovascular manifestations in hypothyroidism have not yet been investigated. We induced experimental hypothyroidism in Psammomys obesus by administering carbimazole for five months. At the end of the experiment, the animals were sacrificed and histopathological analysis was performed using Masson's trichrome staining of the aorta and thyroid gland. The expression of the Agt gene and the genes implicated in cholesterol metabolism regulation in the liver and VSMCs was determined by qRT-PCR. Histological observations revealed profound remodeling of the aorta structure in animals with hypothyroidism. In addition, Agt gene expression in the liver was significantly increased. In vitro study, showed that VSMCs from hypothyroid animals overexpressed 3-hydroxy-3-methylglutaryl coenzyme A reductase ( Hmgcr ) and Acyl CoA:cholesterol acyltransferase ( Acat ) 1, with failure to increase the efflux pathway genes (ATP-binding cassette subfamily G member ( Abcg) 1 and 4 ). These results suggest that hypothyroidism leads to vascular alterations, including structural remodeling, VSMCs cholesterol metabolism dysfunction, and their switch to a synthetic phenotype, together with hepatic Agt gene overexpression.

Since the increasing prevalence of obesity is one of the major health problems of the modern era, understanding the mechanisms of oro-gustatory detection of dietary fat is critical for the prevention and treatment of obesity. We have conducted the present study on Psammomys obesus, the rodent desert gerbil which is a unique polygenic natural animal model of obesity. Our results show that obese animals exhibit a strong preference for lipid solutions in a two-bottle test. Interestingly, the expression of CD36, a lipido-receptor, in taste buds cells (TBC), isolated from circumvallate papillae, was decreased at mRNA level, but remained unaltered at protein level, in obese animals. We further studied the effects of linoleic acid (LA), a long-chain fatty acid, on the increases in free intracellular calcium (Ca2+) concentrations, [Ca2+]i, in the TBC of P. obesus. LA induced increases in [Ca2+]i, largely via CD36, from intracellular pool, followed by the opening of store-operated Ca2+ (SOC) channels in the TBC of these animals. The action of this fatty acid on the increases in [Ca2+]i was higher in obese animals than that in controls. However, the release of Ca2+ from intracellular stores, studied also by employing thapsigargin, was lower in TBC of obese animals than control rodents. In this study, we show, for the first time, that increased lipid intake and altered Ca2+ signaling in TBC are associated with obesity in Psammomys obesus.

Type 2 diabetes mellitus (T2DM) increases cardiac inflammation which promotes the development of cardiac fibrosis. We sought to determine the impact of circadian disruption on the induction of hyperglycaemia, inflammation and cardiac fibrosis. Methods: Psammomys obesus ( P. obesus ) were exposed to neutral (12 h light:12 h dark) or short (5 h light:19 h dark) photoperiods and fed a low energy (LE) or high energy (HE) diet for 8 or 20 weeks. To determine daily rhythmicity, P. obesus were euthanised at 2, 8, 14, and 20 h after ‘lights on’. Results: P. obesus exposed to a short photoperiod for 8 and 20 weeks had impaired glucose tolerance following oral glucose tolerance testing, compared to a neutral photoperiod exposure. This occurred with both LE and HE diets but was more pronounced with the HE diet. Short photoperiod exposure also increased myocardial perivascular fibrosis after 20 weeks on LE (51%, P  < 0.05) and HE (44%, P  < 0.05) diets, when compared to groups with neutral photoperiod exposure. Short photoperiod exposure caused elevations in mRNA levels of hypertrophy gene Nppa (atrial natriuretic peptide) and hypertrophy transcription factors Gata4 and Mef2c in myocardial tissue after 8 weeks. Conclusion: Exposure to a short photoperiod causes impaired glucose tolerance in P. obesus that is exacerbated with HE diet and is accompanied by an induction in myocardial perivascular fibrosis.

3,5-Diiodothyronine (3,5-T2) has been shown to exert pleiotropic beneficial effects. In this study we investigated whether 3,5-T2 prevent several energy metabolism disorders related to type 2 diabetes mellitus (T2DM) in gerbils diabetes-prone P. obesus. 157 male gerbils were randomly to Natural Diet (ND-controlled) or a HED (High-Energy Diet) divided in: HED- controlled, HED-3,5-T2 and HED- Placebo groups. 3,5-T2 has been tested at 25 µg dose and was administered under subcutaneous pellet implant during 10 weeks. Isolated hepatocytes were shortly incubated with 3,5-T2 at 10−6 M and 10−9 M dose in the presence energetic substrates. 3,5-T2 treatment reduce visceral adipose tissue, prevent the insulin resistance, attenuated hyperglycemia, dyslipidemia, and reversed liver steatosis in diabetes P. obesus. 3,5-T2 decreased gluconeogenesis, increased ketogenesis and enhanced respiration capacity. 3,5-T2 potentiates redox and phosphate potential both in cytosol and mitochondrial compartment. The use of 3,5-T2 as a natural therapeutic means to regulate cellular energy metabolism. We suggest that 3,5-T2 may help improve the deleterious course of obesity and T2DM, but cannot replace medical treatment.

It is generally accepted that microbial digestion contributes little to digesta particle size reduction in herbivores, and that faecal particle size reflects mainly chewing efficiency, and may vary with diet. Nevertheless, a decrease in mean particle size (MPS) along the gastrointestinal tract (GIT) has been reported, especially in hindgut fermenters. However, to what degree the very fine particle fraction (non-food origin, especially microbes) affects MPS is unclear. Fat sand rats (Psammomys obesus, diurnal herbivores, n = 23, 175 ± sd 24 g) consumed one of four chenopods (natural dietary items in the wild) for 30 days. Digestibility was related negatively to dietary fibre content. We determined digesta MPS in the forestomach, glandular stomach, small intestine, caecum, colon and faeces by wet sieving, including (MPSfines) or excluding (MPSnofines) particles < 0.25 mm. The proportions of fines were higher and of MPSfines were correspondingly lower in GIT sections that harbour microbes (forestomach, hindgut), whereas MPSnofines did not differ between forestomach and glandular stomach. However, MPSnofines decreased along the GIT, indicating MPS reduction due to digestive (enzymatic and microbial) processes. The four different diets led to different MPS, but the magnitude of MPS reduction in the GIT was not correlated with dietary fibre fractions or dry matter digestibility. These results indicate that within a species, MPS cannot be used as a proxy for diet quality or digestibility, and raise the hypothesis that MPS reduction along the GIT may be more pronounced in smaller than in larger mammalian terrestrial herbivores, possibly due to the fine initial particles produced by chewing in small species.

Psammomys obesus gerbils are particularly prone to develop diabetes and obesity after brief period of abundant food intake. A hypercaloric high fat diet has been shown to affect cardiac function. Here, we sought to determine whether a short period of high fat feeding might alter myocardial structure and expression of calcium handling proteins in this particular strain of gerbils. Twenty Psammomys obesus gerbils were randomly assigned to receive a normal plant diet (controls) or a high fat diet. At baseline and 16-week later, body weight, plasma biochemical parameters (including lipid and carbohydrate levels) were evaluated. Myocardial samples were collected for pathobiological evaluation. Sixteen-week high fat dieting resulted in body weight gain and hyperlipidemia, while levels of carbohydrates remained unchanged. At myocardial level, high fat diet induced structural disorganization, including cardiomyocyte hypertrophy, lipid accumulation, interstitial and perivascular fibrosis and increased number of infiltrating neutrophils. Myocardial expressions of pro-apoptotic Bax-to-Bcl-2 ratio, pro-inflammatory cytokines [interleukin (IL)-1β and tumor necrosis factor (TNF)-α], intercellular (ICAM1) and vascular adhesion molecules (VCAM1) increased, while gene encoding cardiac muscle protein, the alpha myosin heavy polypeptide (MYH6), was downregulated. Myocardial expressions of sarco(endo)plasmic calcium-ATPase (SERCA2) and voltage-dependent calcium channel (Cacna1c) decreased, while protein kinase A (PKA) and calcium-calmodulin-dependent protein kinase (CaMK2D) expressions increased. Myocardial expressions of ryanodine receptor, phospholamban and sodium/calcium exchanger (Slc8a1) did not change. We conclude that a relative short period of high fat diet in Psammomys obesus results in severe alterations of cardiac structure, activation of inflammatory and apoptotic processes, and altered expression of calcium-cycling determinants.

The passage of food through the digestive tract in an herbivorous rodent with a single-chamber semiglandular stomach, the fat sand rat Psammomys obesus, was studied by multiple marking of the food with inert plastic markers. The total mean retention time of markers in the digestive tract (DT), as well as in the stomach and caecum separately, was determined. The peculiarities of the digesta kinetics depending on the morphology of the digestive tract, diet, and the time of marker intake were clarified. The total time for removal of markers from the DT in the fat sand rat reaches 36 h. The mean retention time of markers in the DT was determined as a whole (17–18 h), as well as separately in the forestomach (7–9 h) and caecum (7–12 h). The uneven passage of feed has been revealed, which is considered as an important mechanism for maximizing the extraction of nutrients from plants, including microbial fermentation of structural carbohydrates of the food.

Astaxanthin (ATX) is a marine carotenoid known for its powerful antioxidant and neuroprotective properties. In this study, we investigated the in vitro and in vivo potential inhibitory effect of ATX on the aldose reductase (AR) activity, a key enzyme in the polyol pathway responsible for the pathogenesis of diabetic complications including diabetic retinopathy (DR). The gerbil Psammomys obesus (P. ob.), an animal model for type 2 diabetes and DR has been used. The erythrocyte and retinal AR activity of P. ob. individuals were, respectively, assessed monthly and at the 7th month during a 7‐month hypercaloric diet (HD) using a NADPH oxidation method. Meanwhile, the body weight and blood glucose of the gerbils were monitored. After 7 months, P. ob. individuals were fed with ATX (4.8 mg/kg of body weight) once a day for 1 week. The results showed that the HD‐fed animals developed significant obesity and hyperglycemia in comparison with controls. Erythrocyte AR activity showed a progressive and significant increase in the HD‐fed group compared with controls. Retinal AR activity was higher in the 7‐month HD‐fed group compared with controls. Erythrocyte AR activity was markedly decreased after ATX‐treatment in vitro and in vivo. These findings suggested that ATX inhibited the erythrocyte AR activity and could be used for DR prevention and/or early treatment. We investigated the in vitro and in vivo potential inhibitory effect of astaxanthin on the aldose reductase (AR) activity, a key enzyme in the polyol pathway responsible for the pathogenesis of diabetic complications including diabetic retinopathy (DR) in Psammomys obesus. Our results showed that astaxanthin may prevent and treat diabetes complications.

Rodents, thriving in human-altered environments, pose significant public health risks due to their role as reservoirs for numerous zoonotic parasites. Among these, spp. are recognized globally as leading causes of waterborne and foodborne diarrheal illnesses in humans. The specific role of fat sand rats ( ) in the transmission of spp. in Egypt and the genotypic characteristics of the circulating species in these animals remain poorly understood. In this study, a total of 150 individual fat sand rat stool samples were collected from the saline marsh periurban areas of Abu-Rawash, Giza, Egypt. The samples were initially screened for the presence of spp. using light and scanning electron microscopy to characterize the parasite's oocysts. Furthermore, molecular identification and characterization of the parasite were carried out on selected microscopy-positive samples (  = 30) using conventional polymerase chain reaction (PCR) targeting the oocyst wall protein (COWP) gene. A subset of these positive samples by PCR was subjected to sequencing, with the resulting sequences deposited in GenBank™ and analyzed through phylogenetic methods. Conventional microscopy revealed that 46.7% (70/150; 95% CI: 38.7-54.6) of the analyzed stool samples contained structures consistent with oocysts. Moreover, the molecular analysis confirmed species in DNA from all 30 stool samples previously identified as heavily infected through microscopy. Notably, the phylogenetic analysis identified ( ) in the sequenced samples, likely originating from the rats' native habitats. These identified species have been deposited in GenBank™ under the accession numbers OM817461 ( FSA-1), OM817462 ( FSA-2), and OM817463 ( FSA-3) and revealed closed genetic identity with those species reported from human and other animal species in the same geographic location. Overall, this study represents the first morphological and genetic identification of isolated from fecal samples of fat sand rats trapped from periurban areas in Egypt. These findings provide valuable insights into the potential zoonotic implications of rodents in disease transmission at the national level, offering crucial information for public health awareness campaigns and informing local authorities.