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Introduction: Klebsiella pneumoniae is an opportunistic pathogen that causes a range of diseases. The appearance of extended-spectrum β-lactamase -and carbapenemase-producing strains, in addition to the biofilm-forming phenotype, is a major problem in the clinical environment. Methodology: A total of 33 clinical K. pneumoniae isolates were used in this study. Antimicrobial susceptibilities were assessed by a disc diffusion assay. Biofilm formation was determined by a microtiter plate assay, staining with 1% crystal violet and measuring  absorbance after destaining. Moreover, expression of acrA, kdeA, ketM, kpnEF, and kexD efflux associated genes  was measured by qRT-PCR. Results: Isolates displayed high resistance to β-lactams such as cefazolin, cefuroxime, ceftriaxone, cefepime, piperacillin-tazobactam, imipenem, and meropenem and decreased resistance to gentamicin, amikacin, ciprofloxacin, and levofloxacin. ESBL-producing isolates formed more biofilm than carbapenemase-producing isolates. The mRNA expression levels in KPC isolates for acrA (2-fold), kdeA (2.7-fold), ketM (2.2-fold), and kpnEF (3.4-fold) were significantly increased compared to ESBL-producing isolates. There was no significant difference in kexD expression level. Conclusions: Under the conditions used here ESBL-producing isolates formed more biofilm than KPC postive isolates; this was associated with virulence determinants which were also transferred by plasmids together with ESBLs enzymes. Moreover, the upregulation of acrA, kdeA, ketM, and kpnEF efflux pumps was seen in carbapenemase-producing isolates demonstrating that high expression of efflux pumps alone could not confer resistance but may act as a physiological determinant such as bacterial pathogenicity and virulence, and cell-to-cell communication for bacteria.

Spexin (SPX) is a 14 amino acid length peptide hormone which was discovered using bioinformatic tools. It is extensively expressed in central and peripheral tissues and secreted into circulation in response to metabolic stress. Recent studies revealed that SPX acts as a multifunctional peptide in various metabolic processes such as body weight, food intake, energy balance, glucose and lipid metabolism, lipid storage, salt–water balance, and arterial blood pressure. Endogenous SPX is sensitive to metabolic changes, and circulating levels of SPX have been shown to be reduced in chronic diseases such as obesity, diabetes, and insulin resistance. Moreover, in fish and rodent models, systemic SPX treatment has positive effects on metabolism including reduced food intake, fat mass, lipid accumulation, and inflammation, improved insulin sensitivity, energy expenditure, and organ functions which are underlying mechanisms in diseases. Taken together, these findings suggest that SPX is a potential drug target for the development of new pharmacological strategies to cure metabolic diseases. This review focuses on metabolo-protective properties of SPX and discusses novel insights into the biology and mechanism of SPX in the pathogenesis of diabetes, obesity, non-alcoholic fatty liver disease, metabolic syndrome, polycystic ovary syndrome, cardiovascular diseases, and kidney diseases, which are considerable global health problems.

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