AbstractBackgroundManaging drug–food interactions may help to achieve the optimal action and safety profile of β-lactam antibiotics.MethodsWe conducted a systematic review with meta-analyses in adherence to PRISMA guidelines for 32 β-lactams. We included 166 studies assessing the impact of food, beverages, antacids or mineral supplements on the pharmacokinetic (PK) parameters or PK/pharmacodynamic (PK/PD) indices.ResultsEighteen of 25 β-lactams for which data on food impact were available had clinically important interactions. We observed the highest negative influence of food (AUC or Cmax decreased by >40%) for ampicillin, cefaclor (immediate-release formulations), cefroxadine, cefradine, cloxacillin, oxacillin, penicillin V (liquid formulations and tablets) and sultamicillin, whereas the highest positive influence (AUC or Cmax increased by >45%) for cefditoren pivoxil, cefuroxime and tebipenem pivoxil (extended-release tablets). Significantly lower bioavailability in the presence of antacids or mineral supplements occurred for 4 of 13 analysed β-lactams, with the highest negative impact for cefdinir (with iron salts) and moderate for cefpodoxime proxetil (with antacids). Data on beverage impact were limited to 11 antibiotics. With milk, the extent of absorption was decreased by >40% for cefalexin, cefradine, penicillin G and penicillin V, whereas it was moderately increased for cefuroxime. No significant interaction occurred with cranberry juice for two tested drugs (amoxicillin and cefaclor).ConclusionsFactors such as physicochemical features of antibiotics, drug formulation, type of intervention, and patient’s health state may influence interactions. Due to the poor actuality and diverse methodology of included studies and unproportionate data availability for individual drugs, we judged the quality of evidence as low.

01 Nov 2023·Scandinavian Journal of Medicine & Science in Sports

Vitamin D deficiency contributes to overtraining syndrome in excessive trained C57BL/6 mice

Article

Author: Patrac, V ; Ouchchane, L ; Talvas, J ; Richard, R ; Burban, E ; le Bacquer, O ; Giraudet, C ; Salles, J ; Rigaudière, J-P ; Norgieux, C ; Capel, F ; Walrand, S

AbstractOvertraining syndrome is a condition resulting from excessive training load associated with inadequate recovery and poor sleep quality, leading to performance decrements and fatigue. Here we hypothesized that vitamin D (VitD) deficiency is a lead factor in the development of the overtraining syndrome. To test this hypothesis, two groups of 60‐week‐old C57BL/6 mice followed a 16‐week excessive eccentric‐based overtraining by excessive downhill running with or without dietary VitD depletion (EX and EX‐D− groups). Two control groups were trained by uphill running at the same load with or without VitD depletion (CX and CX‐D− groups). Handgrip strength decreased throughout the protocol for all groups but the decrease was sharper in EX‐D− group (VitD × training, p = 0.0427). At the end of the protocol, the mass of Triceps brachii muscle, which is heavily stressed by eccentric contractions, was reduced in eccentric‐trained groups (training effect, p = 0.0107). This atrophy was associated with a lower concentration of the anabolic myokine IL‐15 (training effect, p = 0.0314) and a tendency to a higher expression of the atrogene cathepsin‐L (training effect, p = 0.0628). VitD depletion led to a 50% decrease of the fractional protein synthesis rate in this muscle (VitD effect, p = 0.0004) as well as decreased FGF21 (VitD effect, p = 0.0351) and increased osteocrin (VitD effect, p = 0.038) concentrations that would lead to metabolic defects. Moreover, the proportion of anti‐inflammatory Th2 lymphocytes was significantly decreased by the combination of eccentric training with VitD depletion (vitD × training, p = 0.0249) suggesting a systemic inflammation. Finally, exploratory behavior time of mice was decreased by VitD depletion (VitD effect, p = 0.0146) suggesting a cognitive dysfunction. Our results suggest that VitD deficiency exacerbates the effects of overtraining.

01 Jan 2020·EBioMedicineQ1 · MEDICINE

The metabolic footprint during adipocyte commitment highlights ceramide modulation as an adequate approach for obesity treatment

Q1 · MEDICINE

ArticleOA

Author: Deng, Chu-Xia ; Qiu, Pengxiang ; Chinn, Y Eugene ; Wang, Haitao ; Lyu, Xueying ; Hou, Weilong ; Chen, Qiang ; Wang, Ruihong ; Chua, Melvin L K ; Chen, Weiping

BACKGROUNDMetabolic modulation is capable of maintaining cell potency, regulating niche homeostasis, or determining cell fate. However, little is known regarding the metabolic landscape during early adipogenesis or whether metabolic modulation could be a potential approach for obesity treatment.METHODSThe metabolic footprint during adipocyte commitment was evaluated by metabolomics analysis in mouse embryonic fibroblasts (MEFs). The role of apoptosis induced by ceramide and how ceramide is regulated were evaluated by omics analysis in vitro, human database and the adipocyte-specific Sirt1 knockout mouse.FINDINGSThe metabolic footprint showed that a complicated diversity of metabolism was enriched as early as 3 h and tended to fluctuate throughout differentiation. Subsequently, the scale of these perturbed metabolic patterns was reduced to reach a balanced state. Of high relevance is the presence of apoptosis induced by ceramide accumulation, which is associated with metabolic dynamics. Interestingly, apoptotic cells were not merely a byproduct of adipogenesis but rather promoted the release of lipid components to facilitate adipogenesis. Mechanistically, ceramide accumulation stemming from hydrolysis and the de novo pathway during early adipogenesis is regulated by Sirt1 upon epigenetic alterations of constitutive Histone H3K4 methylation and H3K9 acetylation.INTERPRETATIONThe metabolic footprint during adipocyte commitment highlights that apoptosis induced by ceramide is essential for adipogenesis, which is reversed by suppression of Sirt1. Therefore, Sirt1 may constitute a target to treat obesity or other ceramide-associated metabolic syndromes.FUNDINGThis project was supported by grants from the University of Macau (SRG2015-00008-FHS, MYRG2016-00054-FHS and MYRG2017-00096-FHS to RHW; CPG2019-00019-FHS to CXD) and from the National Natural Science Foundation of China (81672603 and 81401978) to QC.

100 Deals associated with Cefroxadine

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-	Cefroxadine	J01DB11	DB11367

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Indication	Country/Location	Organization	Date
Bacterial Infections	JP	Alfresa Pharma Corp.	15 Dec 1982

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