Kidney Adaptations Prevent Loss of Trace Elements in Wistar Rats with Early Metabolic Syndrome.

Metabolic syndrome (MetS) represents a cluster of related metabolic abnormalities, including central obesity, hypertension, dyslipidemia, hyperglycemia, and insulin resistance. These metabolic derangements present significant risk factors for chronic kidney disease that carries to loss of essential micronutrients, which accelerates comorbidity apparition. The work aimed was to evaluate the trace element homeostasis regarding morphological adaptations and renal function in MetS early-onset. Fifty male Wistar rats were divided into two groups: (a) control group and (b) hypercaloric diet group that developed MetS early-onset after 3 months. Classical zoometric parameters do not show changes; however, biochemical modifications were observed such as hyperglycemia, protein glycation, insulin resistance, dyslipidemia, hyperinsulinemia, and hypoadiponectinemia. MetS early-onset group observed renal structural modifications, but no functional changes. The structural modifications observed were minimal glomerular injury, glomerular basement membrane thickening, as well as mesangial and tubular cells that showed growth and proliferation. In serum and kidney (cortex and medulla), the concentrations of Zn, Fe, Cr, Mg, Mn, Cu, Co, and Ni were no differences between the experimental groups, but excretory fractions of these were lower in the hypercaloric diet group. In conclusion, MetS early-onset coexist renal structural modification and a hyperreabsorptive activity of essential trace elements that avoid its loss; thus, the excretory fraction of oligo-elements could be used a biomarker of early renal injury caused by metabolic diseases in the clinical practice.

The NOAEL Metformin Dose Is Ineffective against Metabolic Disruption Induced by Chronic Cadmium Exposure in Wistar Rats.

Previous studies have proposed that cadmium (Cd) is a metabolic disruptor, which is associated with insulin resistance, metabolic syndrome, and diabetes. This metal is not considered by international agencies for the study of metabolic diseases. In this study, we investigate the effect of metformin on Cd-exposed Wistar rats at a lowest-observed-adverse-effect level (LOAEL) dose (32.5 ppm) in drinking water. Metabolic complications in the rats exposed to Cd were dysglycemia, insulin resistance, dyslipidemia, dyslipoproteinemia, and imbalance in triglyceride and glycogen storage in the liver, muscle, heart, kidney, and adipose tissue. Meanwhile, rats treated orally with a No-observable-adverse-effect level (NOAEL) dose of metformin (200 mg/kg/day) showed mild improvement on serum lipids, but not on glucose tolerance; in tissues, glycogen storage was improved, but lipid storage was ineffective. In conclusion, metformin as a first-line pharmacological therapy must take into consideration the origin and duration of metabolic disruption, because in this work the NOAEL dose of metformin (200 mg/kg/day) showed a limited efficiency in the metabolic disruption caused by chronic Cd exposure.

Hepatic mobilization of zinc after an experimental surgery, and its relationship with inflammatory cytokines release, and expression of metallothionein and Zip14 transporter.

OBJECTIVE: To study the relationship between the release of inflammatory cytokines and mobilization of zinc into liver, and the expression of metallothionein and Zip14 transporter after an abdominal surgery in rats. MATERIALS: Thirty-five male Wistar rats were subjected to experimental surgical stress, then the subgroups of five animals were killed at 3, 6, 9, 12, 16, 20 and 24 h. Matched groups without surgery were used as controls. METHODS: Zinc levels were determined by AAS, intracellular zinc by zinquin and dithizone staining. Hepatic metallothionein was assayed by a Cd-saturation method, and IL-1ß, IL-6, and TNF-ß by immunoassays. Zip14 expression was analyzed by real-time RT-PCR, and protein level by immunohistochemistry and Western blot. RESULTS: Experimental surgery produced a hypozincemia, and the increase of hepatic zinc also produced the release of IL-1ß, IL-6 in serum, and the increase of hepatic MT. Histochemistry showed a decrease of free zinc at 3-6 h, but an increase at 9 h (zinquin); meanwhile, total intracellular zinc increased after 9 h (dithizone). RNAm and protein levels of Zip14 were elevated between 6 and 20 h after surgery. CONCLUSION: Biochemical changes described in this work could be part of the APR, and directed to respond to the damage produced during surgical trauma.

(R)-3,4,5-Tride-oxy-5,6-didehydro-1,2-O-(2,2,2-trichloro-ethyl-idene)-α-d-gluco-furan-ose-6,3-carbolactone: a new derivative of α-chloralose.

THE TITLE COMPOUND [SYSTEMATIC NAME: (R)-2-trichloro-methyl-3a,3b,7a,8a-tetra-hydro-5H-pyrano[2',3':4,5]furano[2,3-d][1,3]dioxol-5-one], C(9)H(7)Cl(3)O(5), a triyclic system that contains a central α-d-furan-ose ring cis-fused with a dioxolane ring as well as a δ-lactone ring, exhibits a twisted conformation. The CCl(3) group has an axial orientation. The furan-ose ring approximates an envelope conformation due to the α,ß-unsaturated lactone functionality. The asymmetric unit contains two independent mol-ecules with almost identical geometries.