Compensatory Response Research Articles

Urban insect bioarks of the 21st century.

Insects exhibit divergent biodiversity responses to cities. Many urban populations are not at equilibrium: biodiversity decline or recovery from environmental perturbation is often still in progress. Substantial variation in urban biodiversity patterns suggests the need to understand its mechanistic basis. In addition, current urban infrastructure decisions might profoundly influence future biodiversity trends. Although many nature-based solutions to urban climate problems also support urban insect biodiversity, trade-offs are possible and should be avoided to maximize biodiversity-climate cobenefits. Because insects are coping with the dual threats of urbanization and climate change, there is an urgent need to design cities that facilitate persistence within the city footprint or facilitate compensatory responses to global climate change as species transit through the city footprint.

Increased cerebral blood flow is associated with higher baseline amyloid burden in a cognitively unimpaired population

AbstractBackgroundAs cerebrovascular and Alzheimer’s proteinopathy have previously shown to affect cerebral blood flow (CBF) as well as cognition, CBF could be a potential early hemodynamic biomarker of cognitive decline. Here, we investigated to what extent cardiovascular risk factors and amyloid burden affect CBF in an elderly cognitively unimpaired (CU) population.MethodWe included 153 CU participants (minimal MMSE = 28) from the EMIF‐AD PreclinAD Twin60++ cohort (Table 1), who underwent [18F]flutemetamol PET and arterial spin labeling (ASL) MRI. Amyloid‐PET scans were visually assessed as negative or positive, upon which participants were grouped based on their longitudinal changes in amyloid positivity (visual read groups). Cortical amyloid burden was quantified with the Centiloid method globally and for 4 early amyloid accumulation regions of interest (ROIs). ASL scans were processed and quantified with ExploreASL for total gray matter (GM), and for vascular territories overlapping with the amyloid ROIs (Figure 1). Longitudinal analysis including baseline Centiloid values and yearly CBF change rates (Delta CBF) was performed for 98 participants with longitudinal imaging data available (4.23 years ± 0.43 follow‐up time). Associations between CBF and amyloid — with and without the interaction of vascular risk factors (i.e., Framingham score) — were assessed using generalized estimating equations (GEEs), both for baseline and rates of change measurements. Models were adjusted for age, sex, and twin dependency.ResultWhile no association between amyloid burden and CBF was observed across the cohort, in participants with a high Framingham vascular risk score, higher amyloid was associated with increased CBF, for most ROIs (Table 2, Figure 2). Additionally, precuneus amyloid burden was predictive of CBF change in the corresponding vascular territory (Figure 3). Visual reading shows that subjects with high amyloid burden at baseline had a higher increase of CBF at follow‐up (Stable AB+, Figure 4).ConclusionWe found that the combination of cardiovascular risk and amyloid burden in AD signature regions was associated with increased CBF in CU individuals, which may reflect a vascular or inflammatory compensatory response to early Alzheimer pathology. Future studies may help understanding how these mechanisms affect cognition.

Extracellular status of thrombospondin-2 in type 2 diabetes mellitus and utility as a biomarker in the determination of early diabetic kidney disease

ObjectiveThrombospondin-2 (TSP-2) is a multifunctional matricellular glycoprotein correlated with glucose homeostasis, insulin sensitivity, and estimated glomerular filtration rate. Investigation of the association of TSP-2 with type 2 diabetes mellitus (T2DM) and the potential diagnostic value of serum TSP-2 for detecting early diabetic kidney disease (DKD) is needed.Research design and methodsAn enzyme-linked immunosorbent assay was used for detection serum TSP-2 levels in 494 Chinese T2DM subjects. The protein expression of TSP-2 in the kidney and other tissues were tested by western blotting.ResultsSerum TSP-2 levels in T2DM subjects were significantly higher than in healthy individuals. Serum TSP-2 correlated positively with triglycerides, serum uric acid, creatinine, platelets, and urinary albumin-to-creatinine ratio (UACR), but negatively with estimated glomerular filtration rate, after adjusting for age, sex, and T2DM duration. Logistic regression analysis demonstrated an independent association between serum TSP-2 and early DKD. Furthermore, the high UACR identified at risk of early DKD increased significantly from 0.78 (95%CI 0.73–0.83) to 0.82 (95%CI 0.77–0.86, p < 0.001) when added to a clinical model consisting of TSP-2 and age. In db/db mice, serum TSP-2 levels were elevated. TSP-2 expression was markedly increased in the kidney tissue compared with that in db/m and m/m mice. Furthermore, serum TSP-2 expression correlated well with UACR in mice.ConclusionsTSP-2 is a novel glycoprotein associated with early DKD in patients with T2DM. The paradoxical increase of serum TSP-2 in T2DM individuals may be due to a compensatory response to chronic inflammatory and renal vascular endothelial growth, warranting further investigation.

Vestibular feedback for flight control in hawkmoths

Flying insects require mechanosensory feedback to rapidly generate compensatory responses to unexpected perturbations. Such feedback is critical in insects such as moths, which fly under low light levels, compromising their ability to visually compensate for aerial perturbations. Here, we describe how diverse mechanosensory organs have adapted to provide vestibular feedback in various insects, with particular focus on hawkmoths.

Genetic, vascular and amyloid components of cerebral blood flow in a preclinical population

Aging-related cognitive decline can be accelerated by a combination of genetic factors, cardiovascular and cerebrovascular dysfunction, and amyloid-β burden. Whereas cerebral blood flow (CBF) has been studied as a potential early biomarker of cognitive decline, its normal variability in healthy elderly is less known. In this study, we investigated the contribution of genetic, vascular, and amyloid-β components of CBF in a cognitively unimpaired (CU) population of monozygotic older twins. We included 134 participants who underwent arterial spin labeling (ASL) MRI and [18F]flutemetamol amyloid-PET imaging at baseline and after a four-year follow-up. Generalized estimating equations were used to investigate the associations of amyloid burden and white matter hyperintensities with CBF. We showed that, in CU individuals, CBF: 1) has a genetic component, as within-pair similarities in CBF values were moderate and significant (ICC > 0.40); 2) is negatively associated with cerebrovascular damage; and 3) is positively associated with the interaction between cardiovascular risk scores and early amyloid-β burden, which may reflect a vascular compensatory response of CBF to early amyloid-β accumulation. These findings encourage future studies to account for multiple interactions with CBF in disease trajectory analyses.

Impairment of Mesenteric Perfusion as a Marker of Major Bleeding in Trauma Patients.

The majority of potentially preventable mortality in trauma patients is related to bleeding; therefore, early recognition and effective treatment of hemorrhagic shock impose a cardinal challenge for trauma teams worldwide. The reduction in mesenteric perfusion (MP) is among the first compensatory responses to blood loss; however, there is no adequate tool for splanchnic hemodynamic monitoring in emergency patient care. In this narrative review, (i) methods based on flowmetry, CT imaging, video microscopy (VM), measurement of laboratory markers, spectroscopy, and tissue capnometry were critically analyzed with respect to their accessibility, and applicability, sensitivity, and specificity. (ii) Then, we demonstrated that derangement of MP is a promising diagnostic indicator of blood loss. (iii) Finally, we discussed a new diagnostic method for the evaluation of hemorrhage based on exhaled methane (CH4) measurement. Conclusions: Monitoring the MP is a feasible option for the evaluation of blood loss. There are a wide range of experimentally used methodologies; however, due to their practical limitations, only a fraction of them could be integrated into routine emergency trauma care. According to our comprehensive review, breath analysis, including exhaled CH4 measurement, would provide the possibility for continuous, non-invasive monitoring of blood loss.

Functional screening of lysosomal storage disorder genes identifies modifiers of alpha-synuclein neurotoxicity.

Heterozygous variants in the glucocerebrosidase (GBA) gene are common and potent risk factors for Parkinson's disease (PD). GBA also causes the autosomal recessive lysosomal storage disorder (LSD), Gaucher disease, and emerging evidence from human genetics implicates many other LSD genes in PD susceptibility. We have systemically tested 86 conserved fly homologs of 37 human LSD genes for requirements in the aging adult Drosophila brain and for potential genetic interactions with neurodegeneration caused by α-synuclein (αSyn), which forms Lewy body pathology in PD. Our screen identifies 15 genetic enhancers of αSyn-induced progressive locomotor dysfunction, including knockdown of fly homologs of GBA and other LSD genes with independent support as PD susceptibility factors from human genetics (SCARB2, SMPD1, CTSD, GNPTAB, SLC17A5). For several genes, results from multiple alleles suggest dose-sensitivity and context-dependent pleiotropy in the presence or absence of αSyn. Homologs of two genes causing cholesterol storage disorders, Npc1a / NPC1 and Lip4 / LIPA, were independently confirmed as loss-of-function enhancers of αSyn-induced retinal degeneration. The enzymes encoded by several modifier genes are upregulated in αSyn transgenic flies, based on unbiased proteomics, revealing a possible, albeit ineffective, compensatory response. Overall, our results reinforce the important role of lysosomal genes in brain health and PD pathogenesis, and implicate several metabolic pathways, including cholesterol homeostasis, in αSyn-mediated neurotoxicity.

The Role of Inflammation in Age-Associated Changes in Red Blood System.

Aging-related anemia contributes to frailty syndrome, cognitive decline and early mortality. The study aim was to evaluate inflammaging in relation to anemia as a prognostic indicator in affected older patients. The participants (73.0 ± 7.2 years) were allocated into anemic (n = 47) and non-anemic (n = 66) groups. The hematological variables RBC, MCV, MCH, RDW, iron and ferritin were significantly lower, whereas erythropoietin EPO and transferrin Tf tended toward higher values in the anemic group. Approx. 26% of individuals demonstrated transferrin saturation TfS < 20%, which clearly indicates age-related iron deficiency. The cut-off values for pro-inflammatory cytokine IL-1β, TNFα and hepcidin were 5.3 ng/mL, 97.7 ng/mL and 9.4 ng/mL, respectively. High IL-1β negatively affected Hb concentration (rs = -0.581, p < 0.0001). Relatively high odds ratios were observed for IL-1β (OR = 72.374, 95%Cl 19.688-354.366) and peripheral blood mononuclear cells CD34 (OR = 3.264, 95%Cl 1.263-8.747) and CD38 (OR = 4.398, 95%Cl 1.701-11.906), which together indicates a higher probability of developing anemia. The results endorse the interplay between inflammatory status and iron metabolism and demonstrated a high usefulness of IL-1β in identification of the underlying causes of anemia, while CD34 and CD38 appeared useful in compensatory response assessment and, in the longer term, as part of a comprehensive approach to anemia monitoring in older adults.

CMTM3 deficiency induces cardiac hypertrophy by regulating MAPK/ERK signaling

ObjectivesCardiac hypertrophy is the heart's compensatory response stimulated by various pathophysiological factors. However, prolonged cardiac hypertrophy poses a significant risk of progression to heart failure, lethal arrhythmias, and even sudden cardiac death. For this reason, it is crucial to effectively prevent the occurrence and development of cardiac hypertrophy. CMTM is a superfamily of human chemotaxis, which is involved in immune response and tumorigenesis. CMTM3 expressed widely in tissues, including the heart, but its cardiac function remains unclear. This research aims to explore the effect and mechanism of CMTM3 in the development of cardiac hypertrophy. Methods and resultsWe generated a Cmtm3 knockout mouse model (Cmtm3−/−) as the loss-of-function approach. CMTM3 deficiency induced cardiac hypertrophy and further exacerbated hypertrophy and cardiac dysfunction stimulated by Angiotensin Ⅱ infusion. In Ang Ⅱ-infusion stimulated hypertrophic hearts and phenylephrine-induced hypertrophic neonatal cardiomyocytes, CMTM3 expression significantly increased. However, adenovirus-mediated overexpression of CMTM3 inhibited the hypertrophy of rat neonatal cardiomyocytes induced by PE stimulation. In terms of mechanism, RNA-seq data revealed that Cmtm3 knockout-induced cardiac hypertrophy was related to MAPK/ERK activation. In vitro, CMTM3 overexpression significantly inhibited the increased phosphorylation of p38 and ERK induced by PE stimulation. ConclusionsCMTM3 deficiency induces cardiac hypertrophy and aggravates hypertrophy and impaired cardiac function stimulated by angiotensin Ⅱ infusion. The expression of CMTM3 increases during cardiac hypertrophy, and the increased CMTM3 can inhibit further hypertrophy of cardiomyocytes by inhibiting MAPK signaling. Thus, CMTM3 plays a negative regulatory effect in the occurrence and development of cardiac hypertrophy.

109 Effects of Fat-Rich Nutrients in the Pancreas of an Experimental Burn Model

Abstract Introduction Oversupply of nutrients overstimulates beta cells in standard conditions, and severe burn injuries increase the metabolic needs. In this study, we investigated the effects of fat-rich nutrients on the endocrine pancreas during the acute phase of severe burns. Methods Twenty-one Wistar albino rats were randomly divided into 3 groups. Two groups were fed with standard commercial rat chow (1 with sham procedure and 1 with burn procedure), and the third group (also with burn procedure) was fed a fat-rich diet (60% kcal fat). The burn procedure involved a 25% total body surface area fullthickness burn. Blood samples were taken at 36 hours and 7 days after burn injury or sham procedure. On postburn day 7, skin biopsies were taken and a pancreatectomy was performed. Pancreatic tissues were examined under light microscopy; islets size and cellularity were calculated and investigated immunohistochemically. Results Plasma glucose, C-Peptide, and insulin levels were similar in all the study groups 36 hours and 7 days after burn induction or sham procedure. There was a significant increase in the number of cells per one islet in the burn group given a fat-rich diet compared with the other groups (P = .05). Caspase-3 was strongly expressed in both groups with burn injuries. Conclusions Overconsumption of certain fats can lead to a compensatory response by beta cells that eventually can progress to beta-cell dysfunction during the acute phase of burns. Severe burns induce pancreatic islet cell hyperplasia. Providing excessive fat nutrients during the acute postburn period attenuates this response. Despite the morphophysiological changes observed in the pancreas, all animals in our study achieved similar glycemic homeostasis. Applicability of Research to Practice The delivery of nutritional support is a vital element of burn care, and the main goal is simply to avoid nutritional complications. Lipotoxicity contributes to multisystem organ failure and worse clinical outcomes in obese patients and mice with pancreatitis. Neutralization of IL-1β produces beneficial effects on postburn glycemic control and improves survival. apoptosis in the pancreas of patients with severe burns may be linked to a series of events that can induce Caspase-1 activation and IL-1β release, and these pathways may be influenced by the nutritional status, especially in the early postburn phase. Effective nutritional assessment and management can optimize wound healing and decrease complications and mortality.

Peripheral modulation of antidepressant targets MAO-B and GABAAR by harmol induces mitohormesis and delays aging in preclinical models

Reversible and sub-lethal stresses to the mitochondria elicit a program of compensatory responses that ultimately improve mitochondrial function, a conserved anti-aging mechanism termed mitohormesis. Here, we show that harmol, a member of the beta-carbolines family with anti-depressant properties, improves mitochondrial function and metabolic parameters, and extends healthspan. Treatment with harmol induces a transient mitochondrial depolarization, a strong mitophagy response, and the AMPK compensatory pathway both in cultured C2C12 myotubes and in male mouse liver, brown adipose tissue and muscle, even though harmol crosses poorly the blood–brain barrier. Mechanistically, simultaneous modulation of the targets of harmol monoamine-oxidase B and GABA-A receptor reproduces harmol-induced mitochondrial improvements. Diet-induced pre-diabetic male mice improve their glucose tolerance, liver steatosis and insulin sensitivity after treatment with harmol. Harmol or a combination of monoamine oxidase B and GABA-A receptor modulators extend the lifespan of hermaphrodite Caenorhabditis elegans or female Drosophila melanogaster. Finally, two-year-old male and female mice treated with harmol exhibit delayed frailty onset with improved glycemia, exercise performance and strength. Our results reveal that peripheral targeting of monoamine oxidase B and GABA-A receptor, common antidepressant targets, extends healthspan through mitohormesis.

HIF-1 signaling: an emerging mechanism for mitochondrial dynamics.

A growing emphasis has been paid to the function of mitochondria in tumors, neurodegenerative disorders (NDs), and cardiovascular diseases. Mitochondria are oxygen-sensitive organelles whose function depends on their structural basis. Mitochondrial dynamics are critical in regulating the structure. Mitochondrial dynamics include fission, fusion, motility, cristae remodeling, and mitophagy. These processes could alter mitochondrial morphology, number, as well as distribution, to regulate complicated cellular signaling processes like metabolism. Meanwhile, they also could modulate cell proliferation and apoptosis. The initiation and progression of several diseases, such as tumors, NDs, cardiovascular disease, were all interrelated with mitochondrial dynamics. HIF-1 is a nuclear protein presented as heterodimers, and its transcriptional activity is triggered by hypoxia. It plays an important role in numerous physiological processes including the development of cardiovascular system, immune system, and cartilage. Additionally, it could evoke compensatory responses in cells during hypoxia through upstream and downstream signaling networks. Moreover, the alteration of oxygen level is a pivotal factor to promote mitochondrial dynamics and HIF-1 activation. HIF-1α might be a promising target for modulating mitochondrial dynamics to develop therapeutic approaches for NDs, immunological diseases, and other related diseases. Here, we reviewed the research progress of mitochondrial dynamics and the potential regulatory mechanism of HIF-1 in mitochondrial dynamics.

High and diurnally fluctuating carbon dioxide exposure produces lower mercury toxicity in a marine copepod

Coastal waters have experienced fluctuations in partial pressure of carbon dioxide (pCO2) and mercury (Hg) pollution, yet little is known concerning how natural pCO2 fluctuations affect Hg biotoxicity. Here, a marine copepod Tigriopus japonicus was interactively exposed to different seawater pCO2 (ambient 400, steady elevated 1000, and fluctuating elevated 1000 ± 600 μatm) scenarios and Hg (control, 2 μg/L) treatments for 7 d. The results showed that elevated pCO2 decreased Hg bioaccumulation, and it was even more under fluctuating elevated pCO2 condition. We found energy depletion and oxidative stress under Hg-treated copepods, while combined exposure initiated compensatory response to alleviate Hg toxicity. Intriguingly, fluctuating acidification presented more immune defense related genes/processes in Hg-treated copepods when compared to steady acidification, probably linking with the greater decrease in Hg bioaccumulation. Collectively, understanding how fluctuating acidification interacts with Hg contaminant will become more crucial in predicting their risks to coastal biota and ecosystems.

The rationale for intermittent administration of PTH in the management of mineral and bone disorder of chronic kidney disease.

A major complication of chronic kidney disease is the derangement of mineral metabolism, leading to increased risk of fractures and cardiovascular mortality. Current therapeutic regimens are focused on reducing parathyroid hormone levels caused by secondary hyperparathyroidism, and the active vitamin D metabolite l,25(OH)2D, with limited success. It may be a more effective approach, however, if we could target the delayed response of parathyroid hormone in the early retention of phosphate following loss of renal function.We propose intermittent administration (even in stage 2 chronic kidney disease) of parathyroid hormone, known for its bone anabolic effects compared to the catabolic effects of the continuously elevated parathyroid hormone associated with the hyperparathyroid state, to mitigate the retention of phosphate. This approach may prevent the compensatory responses of the other two major calcium- and phosphate-regulating hormones (FGF-23 and l,25(OH)2D) that lead to further worsening of the derangement of mineral metabolism.In addition to its strong theoretical basis, there are data supporting the need for further research focused on the use of intermittent parathyroid hormone in the management of chronic kidney disease-mineral bone disorder.

Reproductive Success Dynamics Could Limit Precision in Close-Kin Mark–Recapture Abundance Estimation for Atlantic Goliath Grouper (Epinephelus itajara)

Extra-Poisson variance in annual reproductive success can affect the precision of abundance estimates made using ‘close-kin’ mark–recapture procedures. However, empirical evaluation of that variance in natural marine populations can be daunting. Here, a scaling method was used to extend a discrete-time, age-structured model, facilitating investigation of annual and lifetime reproductive success dynamics in Epinephelus itajara. Life tables were synthesized from fishery assessment vital rates and life history measures. For model scaling, a precise empirical estimate of effective population size for the studied population was utilized as the independent variable, and model sensitivity to an informative range of adult abundance was evaluated. The potential for sex reversal to impact reproductive success dynamics was also investigated, albeit in the absence of selective fishing pressure and potential compensatory or depensatory responses. Close-kin relationships in a genetic sample of ~300 adults collected from spawning sites in the Florida Atlantic included numerous full-sibling pairs and multi-sibling families, which is unusual for long-lived, iteroparous marine populations with broadly dispersed larvae. The highly overdispersed reproductive success dynamics modeled for this population and its atypical kinship distribution could have ramifications for planned close-kin mark–recapture analyses. The low observed effective size also has conservation implications. Both issues warrant continued genetic monitoring.

Meibomian Gland Dysfunction in Primary Acquired Nasolacrimal Duct Obstruction.

This study was designed to investigate the influence of primary nasolacrimal duct obstruction (PANDO) on the structure and function of the Meibomian gland and to examine whether it is related to functional failure after dacryocystorhinostomy surgery. Medical records of patients diagnosed as PANDO from August 2021 to February 2022 were retrospectively studied. Results of slit lamp examination, lacrimal drainage test, tear break-up time, anterior segment optical coherence tomography, and meibography were collected. Tear meniscus height, tear break-up time, meiboscore, and lipid layer thickness of tear membrane were parameters compared between the eyes with complete PANDO and the control group. Medical records of 44 patients, therefore 88 eyes were collected, and there were 28 eyes with complete PANDO (total obstruction group), while normal eyes (control group) were 30. Mean tear meniscus height was significantly higher than that of the control group ( P value<0.001), but tear break-up time ( P value=0.322), lipid layer thickness ( P value=0.755), and meiboscore ( P value=0.268) were not significantly different. However, in the cases with moderate and severe meibomian gland destruction, the lipid layer thickness of the total obstruction group was significantly thinner than the control group. Lipid secretion of meibomian glands was less in eyes with PANDO than in eyes without PANDO, under moderate to severe meibomian gland destruction. It can lead to persistent epiphora after dacryocystorhinostomy due to a compensatory response against evaporative dry eye disease. Patients should be educated before the decision to undergo surgeries about the possibilities of persistent epiphora. Further studies are needed to prove the mechanism of meibomian gland function disturbance in PANDO.

A proprioceptive feedback circuit drives Caenorhabditis elegans locomotor adaptation through dopamine signaling

An animal adapts its motor behavior to navigate the external environment. This adaptation depends on proprioception, which provides feedback on an animal's body postures. How proprioception mechanisms interact with motor circuits and contribute to locomotor adaptation remains unclear. Here, we describe and characterize proprioception-mediated homeostatic control of undulatory movement in the roundworm Caenorhabditis elegans. We found that the worm responds to optogenetically or mechanically induced decreases in midbody bending amplitude by increasing its anterior amplitude. Conversely, it responds to increased midbody amplitude by decreasing the anterior amplitude. Using genetics, microfluidic and optogenetic perturbation response analyses, and optical neurophysiology, we elucidated the neural circuit underlying this compensatory postural response. The dopaminergic PDE neurons proprioceptively sense midbody bending and signal to AVK interneurons via the D2-like dopamine receptor DOP-3. The FMRFamide-like neuropeptide FLP-1, released by AVK, regulates SMB head motor neurons to modulate anterior bending. We propose that this homeostatic behavioral control optimizes locomotor efficiency. Our findings demonstrate a mechanism in which proprioception works with dopamine and neuropeptide signaling to mediate motor control, a motif that may be conserved in other animals.

Neurodynamics of Awareness Detection in Tibetan Immigrants: Evidence from Electroencephalography Analysis

The psychological effects of long-term exposure to high-altitude environments have attracted great attention. These effects are usually attributed to the diminished cognitive resources due to high-altitude exposure. This study employed electroencephalography (EEG) to investigate the effects of exposure duration on awareness detection tasks. Neither reaction time nor accuracy showed the direct effects of the exposure duration, so did the model indexes obtained from drift diffusion model analysis. However, event-related potentials (ERP) analysis revealed that exposure duration was associated with changes in the visual awareness negativity (VAN) and the late positivity (LP) components, which in turn affected reaction time. Specifically, longer exposure durations were associated with lower VAN and higher LP, resulting in shorter reaction times and greater drift rate. In contrast to previous studies, the reverse relationship between VAN and LP may reflect a compensatory response to the reduced cognitive resources caused by high-altitude exposure. Additionally, increased LP and shorter reaction times with exposure duration may reflect a resistance to the high-altitude environment. We also conducted time–frequency analysis and found that theta power did not vary with exposure duration, suggesting that the reduction in cognitive resources remains stable in these individuals over time. Overall, our study provides new insights into the dynamic effects of high-altitude environments on awareness detection in the presence of reduced cognitive resources.

Evidence of a compensatory response in invasive Rusty Crayfish (Faxonius rusticus) following intensive harvest removal from northern Lake Michigan fish spawning reefs.

The online version contains supplementary material available at 10.1007/s10530-023-03076-6.

The influence of napier grass biomass mixed feed on the biorefinery indicator for Nile tilapia production.

Aquaculture is vital for feeding a growing population as aquatic creatures require more protein. Utilizing protein-rich biomass for feeding animals is a possible solution. Biorefinery technology can extract protein and non-protein components from biomass, creating an economically feasible value chain. This study replaced fish feed with napier grass and used a compensatory response to reduce the cost of feeding Nile tilapia. The trial involved dividing mono-sex male Nile tilapia, initially weighing between 11.10 and 13.60 g/f, into four groups with three replications based on their feeding regime. Therefore, in the study, four groups of Nile tilapia were fed different diets for 90 days. The control group (T1) received a commercial floating pellet diet throughout the trial. Group T2 and T3 received a mix of commercial floating pellet diet and napier grass in varying proportions, and group T4 was fed with only napier grass throughout the trial. The study found that groups T2 and T3 had remarkable fish growth performance, high digestibility of napier grass, and lower feed prices with the highest benefit-cost ratios. The percentage of edible flesh and Hepatosomatic Index (PT2) were higher in group T2 than T3. Cellulase activity decreased with the frequency of napier grass intake, and the amylase activity was higher in T2 than T3, which also had the highest growth performance and feed utilization. Therefore, the study suggests that the optimal feeding regimen for Nile tilapia is T2 or T3, which promotes growth and is cost-effective.