Exploring diabesity pathophysiology through proteomic analysis using .

Introduction: Diabesity, characterized by obesity-driven Type 2 diabetes mellitus (T2DM), arises from intricate genetic and environmental interplays that induce various metabolic disorders. The systemic lipid and glucose homeostasis is controlled by an intricate cross-talk of internal glucose/insulin and fatty acid molecules to maintain a steady state of internal environment.

Methods: In this study, were maintained to achieve glucose concentrations resembling the hyperglycemic conditions in diabetic patients to delve into the mechanistic foundations of diabesity.

Stress-Induced Eukaryotic Translational Regulatory Mechanisms.

The eukaryotic protein synthesis process entails intricate stages governed by diverse mechanisms to tightly regulate translation. Translational regulation during stress is pivotal for maintaining cellular homeostasis, ensuring the accurate expression of essential proteins is important for survival. This selective translational control mechanism is integral to cellular adaptation and resilience under adverse conditions.

Roles of Progranulin and FRamides in Neural Versus Non-Neural Tissues on Dietary Restriction-Related Longevity and Proteostasis in .

Dietary Restriction (DR) mitigates loss of proteostasis associated with aging that underlies neurodegenerative conditions including Alzheimer's disease and related dementias. Previously, we observed increased translational efficiency of certain FMRFamide-Like neuro-Peptide () genes and the neuroprotective growth factor progranulin gene under dietary restriction in . Here, we tested the effects of , , and on lifespan and proteostasis under both standard and dietary restriction conditions.

Stress-induced Eukaryotic Translational Regulatory Mechanisms.

The eukaryotic protein synthesis process entails intricate stages governed by diverse mechanisms to tightly regulate translation. Translational regulation during stress is pivotal for maintaining cellular homeostasis, ensuring the accurate expression of essential proteins crucial for survival. This selective translational control mechanism is integral to cellular adaptation and resilience under adverse conditions.

Neuronal CBP-1 is required for enhanced body muscle proteostasis in response to reduced translation downstream of mTOR.

Background: The ability to maintain muscle function decreases with age and loss of proteostatic function. Diet, drugs, and genetic interventions that restrict nutrients or nutrient signaling help preserve long-term muscle function and slow age-related decline. Previously, it was shown that attenuating protein synthesis downstream of the mechanistic target of rapamycin (mTOR) gradually increases expression of heat shock response (HSR) genes in a manner that correlates with increased resilience to protein unfolding stress.

Roles of progranulin and FRamides in neural versus non-neural tissues on dietary restriction-related longevity and proteostasis in .

Dietary restriction (DR) mitigates loss of proteostasis associated with aging that underlies neurodegenerative conditions including Alzheimer's disease and related dementias. Previously, we observed increased translational efficiency of certain FMRFamide-like neuropeptide ( ) genes and the neuroprotective growth factor progranulin gene under dietary restriction in . Here, we tested the effects of , , and on lifespan and proteostasis under both standard and dietary restriction conditions.

The integrated stress response protects against ER stress but is not required for altered translation and lifespan from dietary restriction in .

The highly conserved integrated stress response (ISR) reduces and redirects mRNA translation in response to certain forms of stress and nutrient limitation. It is activated when kinases phosphorylate a key residue in the alpha subunit of eukaryotic translation initiation factor 2 (eIF2). General Control Nonderepressible-2 (GCN2) is activated to phosphorylate eIF2α by the presence of uncharged tRNA associated with nutrient scarcity, while protein kinase R-like ER kinase-1 (PERK) is activated during the ER unfolded protein response (UPR).

Anabolic Function Downstream of TOR Controls Trade-offs Between Longevity and Reproduction at the Level of Specific Tissues .

As the most energetically expensive cellular process, translation must be finely tuned to environmental conditions. Dietary restriction attenuates signaling through the nutrient sensing mTOR pathway, which reduces translation and redirects resources to preserve the soma. These responses are associated with increased lifespan but also anabolic impairment, phenotypes also observed when translation is genetically suppressed.

Physiological and Metabolite Alterations Associated with Neuronal Signals of during Infections.

Metabolomic reprogramming plays a crucial role in the activation of several regulatory mechanisms including neuronal responses of the host. In the present study, alterations at physiological and biochemical levels were initially assessed to monitor the impact of the candidate pathogen on the nematode host . The abnormal behavioral responses were observed in infected worms in terms of hyperosmolarity and high viscous chemicals.

Proteomic analysis of Caenorhabditis elegans against Salmonella Typhi toxic proteins.

Bacterial effector molecules are crucial infectious agents that can cause pathogenesis. In the present study, the pathogenesis of toxic Salmonella enterica serovar Typhi (S. Typhi) proteins on the model host Caenorhabditis elegans was investigated by exploring the host's regulatory proteins during infection through the quantitative proteomics approach.

Modulation of the host cell mitochondrial proteome by PemK toxin protein exposure.

Mitochondria are essential organelles involved in abundant cellular functions ranging from energy metabolism to cell survival. The inhibition of these mitochondrial functions by bacterial toxin proteins promotes disease and inhibits cell growth. Prominent evidence proposes that mitochondria provide a platform for innate immune response signalling pathways.

and efficacy of recombinant antimicrobial protein against Gram-negative bacteria.

Antimicrobial peptides (AMPs) are short, positively charged host defense peptides, found in various life forms from microorganisms to humans. AMPs are gaining more attention as substitutes for antibiotics in order to combat the risk posed by multi-drug- resistant pathogens. The nematode relies solely on its innate immune defense to cope with its challenging life-style.

Global Proteomic Response of Against PemK Toxin.

Bacterial exotoxins are major causative agents that infect by promoting cell and tissue damages through disabling the invading host immune system. However, the mode of action by which toxins modulate host immune system and lead cell death is still not completely understood. The nematode, has been used as an attractive model host for toxicological studies.

A proteomic analysis of Caenorhabditis elegans mitochondria during bacterial infection.

Mitochondria are involved in a variety of cellular metabolic processes and their functions are regulated by intrinsic and extrinsic stimuli. Recent studies have revealed functional diversity and importance of mitochondria in many cellular processes, including the innate immune response. This study evaluated the specific response and proteomic changes in host Caenorhabditis elegans mitochondria during Pseudomonas aeruginosa PAO1 infection.