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PubMed2025

Effects of Sodium-Glucose Cotransporter-2 Inhibitors on Modulating Protein-Bound Uremic Toxins and Gut Microbiota in Predialysis CKD Patients: Matched Case-Control Study.

KEY POINTS: A reduction of indoxyl sulfate, p-cresyl sulfate, and several short-chain fatty acids was seen in sodium-glucose cotransporter-2 inhibitor-treated CKD patients. Variations in gut microbiota composition are correlated with levels of gut-derived uremic toxins in sodium-glucose cotransporter-2 inhibitor-treated CKD patients. BACKGROUND: The intricate interplay between CKD and intestinal microbiota has gained increasing attention, with gut dysbiosis being implicated in uremic toxin accumulation and CKD progression. Sodium-glucose cotransporter-2 inhibitors (SGLT2i) are now transforming CKD management but pose uncertain effects on shaping gut microbiota. This study aimed to elucidate the effect of SGLT2i on perturbations of gut microbial composition and metabolic responses in patients with CKD. METHODS: Analysis of fecal microbiota and targeted profiling of serum short-chain fatty acids and gut-derived uremic toxins were conducted in a matched case-control study, including 60 patients with CKD (treated: n=30; untreated: n=30) and 30 non-CKD controls. RESULTS: Gut microbial composition differed significantly among the three study groups. Patients with CKD receiving SGLT2i exhibited distinctive taxonomic profiles, such as enrichment of Bacteroides stercoris and Bacteroides coprocola. Surveys of metabolomic profiles revealed a reduction of two uremic solutes, indoxyl sulfate and p-cresyl sulfate (pCS), and several short-chain fatty acids (formic, acetic, propionic, valeric, and 2-methylbutanoic acid) in SGLT2i-treated CKD patients. Co-occurrence analysis demonstrated a set of intestinal microbes that is positively or negatively correlated with the levels of pCS, and the abundance of these pCS-associated intestinal microorganisms was correlated with the levels of indoxyl sulfate and isovaleric acids in the same and opposite direction, respectively. Further functional prediction indicated attenuated pathways related to protein and carbohydrate metabolism. CONCLUSIONS: Treatment with SGLT2i in patients with CKD is associated with distinct gut microbial composition and metabolite profiles, suggesting potential modulation of gut dysbiosis and metabolic pathways. Further studies are warranted to elucidate the clinical implications of these findings in CKD management.

CKD↗
PubMed1975

[Estradiol-17beta, estrone, LH and FSH in serum after administration of estradiol-17beta, estradiolbenzoate, estradiol-valeriate and estradiol-undecylate in the female (author's transl)].

Estradiol-17beta, estradiol-benzoate, estradiol-valerianate, and estradiol-undecylate were injected intravenously and intramuscularly to postmenopausal woman and to female castrates. Equal doses were used corresponding to 20 mg of free estradiol-17beta. Estradiol-17beta, estrone, FSH and LH were measured in serum by radioimmunoassay before and after application of the hormone and the estradiol esters. Thus the depot effect of the different esters could be compared.

Adult↗
PubMed1990

Excitatory and inhibitory amino-acidergic determinants of the pressure-induced neuronal hyperexcitability in rat hippocampal slices.

In a previous study we found that the intrinsic excitability of the hippocampal CA1 pyramidal cells increased under helium pressure (80 bar). We presently show that drugs inhibiting gamma-aminobutyric acid (GABA) uptake or facilitating GABA binding partially reversed the pressure-induced hyperexcitability of the CA1 pyramidal cells. When these drugs were simultaneously applied with 2-D,L-aminophosphonovaleric acid, a specific antagonist of N-methyl-D-aspartate (NMDA) receptors, the effect of pressure on the neuronal excitability was nearly abolished. These results suggested that the observed pressure-induced hyperexcitability of pyramidal cells resulted from reduced efficiency of GABA transmission and facilitated excitation mediated by NMDA receptors.

Animals↗
PubMed1990

Solid-phase synthesis of peptides with C-terminal asparagine or glutamine. An effective, mild procedure based on N alpha-fluorenylmethyloxycarbonyl (Fmoc) protection and side-chain anchoring to a tris(alkoxy)benzylamide (PAL) handle.

Attempts to anchor Fmoc-asparagine or glutamine as p-alkoxybenzyl esters for solid-phase peptide synthesis are fraught with difficulties. A convenient and effective method to prepare peptides with C-terminal asparagine or glutamine involves quantitative attachment of N alpha-Fmoc-C alpha-tert.-butyl aspartate or glutamate via the free omega-carboxyl groups to a tris(alkoxy)benzylamino (PAL) support. Chain elongation proceeds normally by standard Fmoc chemistry, and treatment with acid, e.g., CF3COOH--CH2Cl2, 90 min at 25 degrees, releases the desired peptides in greater than 95% yields without side reactions at the C-terminus. Feasibility of the approach has been demonstrated by the syntheses of the C-terminal octapeptide from human proinsulin, H-Leu-Ala-Leu-Glu-Gly-Ser-Leu-Gln-OH, and the serum thymic factor pGlu-Ala-Lys-Ser-Gln-Gly-Gly-Ser-Asn-OH.

Amino Acids↗
PubMedDate not supplied

Fanconi syndrome in a patient with a variant of isovaleric acidemia.

Fanconi syndrome with proximal renal tubular acidosis is caused by a variety of anatomic, functional and metabolic disorders. We report a patient with a variant of isovaleric acidosis who developed proximal tubular acidosis. This patient was able to acidify the urine during metabolic acidosis, developed a hyperchloremic metabolic acidosis, and needed 24 mEq/kg/day of bicarbonate to maintain normal serum bicarbonate. She had a FE Bicarbonate of 12 +/- 4% during bicarbonate infusion. Isovaleric acidosis may be another toxic cause of proximal RTA.

Acidosis↗
PubMed1985

The Gemfibrozil Study.

In clinical studies in dyslipidaemic patients gemfibrozil has produced falls in LDL and VLDL of 10-20% and 30-50%, respectively, but a rise in HDL of 15-25%. Gemfibrozil also produces increases in both Apo AI and AII, and in kininogen and prekallikrein. Side-effects are not a major problem. The Helsinki Heart Study has compared the effects of gemfibrozil with those of placebo in a group of 4080 dyslipidaemic Finnish men aged 40-55. The results are not yet available but there is reason to believe that the probable level of coronary risk reduction will be at least as great as that reported by the Lipid Research Clinics Study Coronary Primary Prevention Trial (LRC-CPPT).

Adult↗
PubMed1983

Effects of gemfibrozil on serum lipids.

A two-part, multicenter study to assess the clinical efficacy, side effects, and safety of gemfibrozil in 427 patients over treatment durations of up to 13 months showed that this drug markedly reduces the level of serum triglycerides, while moderately lowering total serum cholesterol levels. The high-density lipoprotein cholesterol level was substantially increased, with concomitant decreases in low-density lipoprotein and very low-density lipoprotein cholesterol levels. The drug was generally well tolerated. However, a potential for increasing blood glucose levels was noted and careful monitoring during therapy is recommended.

Adult↗
PubMed1983

[Isovaleric aciduria].

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Amino Acid Metabolism, Inborn Errors↗