Biology subjects

Sultan, A.

Publications and source records attributed to Sultan, A..

4 recordsLinked to original sources

bioRxiv2025

Proximate Composition and Mineral Analysis of Housefly Maggots and Mealworms Compared to Fish and Soybean Meals

The nutritional profiles of dried yellow mealworms and housefly maggots were analyzed and compared with conventional protein sources in poultry diets such as fish meal (FM) and soybean meal (SBM). Nutrient composition was determined through proximate analysis, while amino acid and mineral contents were analyzed using HPLC-based amino acid analyzer and atomic absorption spectrophotometer, respectively. Metabolizable energy (ME) was calculated to estimate energy content per kilogram of feed. The crude protein content of housefly maggots (57.8%) was comparable to that of fish meal (58.5%), which was the highest among the evaluated feeds, while mealworms had a slightly lower protein content (51.02%). The highest ether extract values were recorded for mealworms (27.3%) and maggots (26.9%), surpassing those in FM and SBM. The highest ME was calculated for housefly maggots (4,074 kcal/kg), followed by mealworms (3,988 kcal/kg) and FM (3,824 kcal/kg). Mineral profiling showed the highest calcium content in mealworms (5.23 g/kg), followed by maggots (5.13 g/kg). Phosphorus and zinc were recorded highest in housefly maggots, at 16.8 g/kg and 98.5 mg/kg, respectively. The limiting amino acids lysine, leucine, and isoleucine were highest in housefly maggots, followed by FM and mealworms, showing comparable values between the insect meals and FM. Methionine content was recorded highest in mealworms (2.3 g/100g), closely followed by housefly maggots (2.27 g/100g). The study demonstrated that housefly maggots and mealworms have a nutritive profile superior to soybean meal and comparable to fish meal.

zoology↗

bioRxiv2024

Obesity induces phenotypic switching of gastric smooth muscle cells through the activation of the PPARD/PDK4/ANGPTL4 pathway

ObjectiveClinical research has identified stomach dysmotility as a common feature of obesity. However, the specific mechanisms driving gastric emptying dysfunction in patients with obesity remain largely unknown. In this study, we investigated potential mechanisms by focusing on the homeostasis of gastric smooth muscle, using tissue samples from both patient and mice, as well as human cell culture system. DesignTissue samples were collected from patients who underwent sleeve gastrectomy for obesity, as well as from control subjects with standard weight who were undergoing treatment for gastric or esophageal carcinoma. Stomach tissues were harvested from mice after 12 weeks on a High-Fat Diet (HFD). Differentiated human gastric smooth muscle cells (SMCs) were treated with lipids, siRNA-peptide-based nanoparticles and/or pharmaceutical compounds. All experimental conditions were analyzed for their effects on SMC differentiation using stage-specific smooth muscle markers. Additionally, lipidomic and RNA sequencing analyses were performed on human gastric SMC cultures. The findings were assessed in patients with obesity to evaluate their clinical relevance. ResultsThe smooth muscle layers in gastric tissue from both patients with obesity and mice fed on a HFD exhibited altered differentiation status. Treatment of differentiated human gastric SMCs with lipids phenocopies these alterations and is associated with increased expression of PDK4 and ANGPTL4. Inhibition of PDK4 or ANGPTL4 upregulation prevents these lipid-induced modifications. Mechanistically, lipid treatment activates PPARD, which regulates PDK4 and ANGPTL4 upregulation, leading to SMC dedifferentiation. Notably, PDK4 and ANGPTL4 levels correlate with immaturity and alteration of gastric smooth muscle in patients with obesity. ConclusionObesity triggers a phenotypic change in gastric SMCs, driven by the activation of the PPARD/PDK4/ANGPTL4 pathway. These mechanistic insights offer potential biomarkers for diagnosing stomach dysmotility in patients with obesity.

physiology↗

bioRxiv2024

Differential effects of obesity and diabetes on the action potential waveform and inward currents in rat ventricular myocytes.

Obesity is a significant health concern worldwide, increasing the risk for type 2 diabetes mellitus (T2DM) and cardiovascular disease. Studies have found various vascular anomalies, abnormal heart rhythm, and impaired electro-mechanical coupling in patients with diabetes. Research on non-diabetic obese individuals has shown that besides diabetes-related complications, obesity itself raises the risk of developing cardiovascular disease. Recent studies have revealed a decrease in the speed of electrical signal conduction in the heart, along with slight gap junction dysfunction, which is insufficient to explain the observed impediment of impulse conduction. Its still unclear whether this impairment is due to obesity-related fat toxicity or diabetes-related factors. Our study aimed to investigate the ventricular action potential parameters and voltage-gated Na+ (INa) and Ca2+ (I(Ca, L)) currents in Zucker fatty (ZF) rats in comparison to Zucker diabetic fatty (ZDF) rats, a well-established model of obesity and T2DM. Ventricular myocytes were enzymatically isolated from 25-30-week-old Zucker rats. Resting and action potentials were recorded from isolated left ventricular myocytes using a {beta}-escin perforated patch clamp in current-clamp mode; INa and I(Ca, L) were recorded using whole-cell patch clamp techniques. Ventricular myocytes from ZF rats showed higher excitability and faster upstroke velocity. ZF rats also had a larger density of INa. Conversely, ZDF rats had decreased INa which correlated with a reduced velocity of the action potential upstroke. There were no changes in the density or voltage sensitivity of I(Ca, L) among the three groups of animals. In conclusion, obesity alone and obesity accompanied by DM have distinct effects on the action potential waveform, INa density and excitability of ventricular myocytes in a rat model of T2DM.

physiology↗

bioRxiv2020

Aberrant gliogenesis and excitation in MEF2C autism patient hiPSC-neurons and cerebral organoids

MEF2C has been shown to be a critical transcription factor for neurodevelopment, whose loss-of-function mutation in humans results in MEF2C haploinsufficiency syndrome (MHS), a severe form of autism spectrum disorder (ASD)/intellectual disability (ID). Here, we use patient hiPSC-derived cerebrocortical neurons and cerebral organoids to characterize MHS deficits. Unexpectedly, we found an aberrant micro-RNA-mediated gliogenesis pathway that contributes to decreased neurogenesis. We also demonstrate network-level hyperexcitability in neurons, as evidenced by excessive synaptic and extrasynaptic activity contributing to excitatory/inhibitory (E/I) imbalance. Notably, the extrasynaptic NMDA receptor antagonist, NitroSynapsin, corrects this aberrant electrical activity associated with abnormal phenotypes. During neurodevelopment, MEF2C regulates many ASD-associated gene networks suggesting that our approach may lead to personalized therapy for multiple forms of ASD. One sentence summaryAutism-like MEF2C+/- patient hiPSC models show miRNA-mediated overproduction of astrocytes and hyperactivity of neurons.

neuroscience↗