PubMed · 13804284
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A BRETON, O POINGT. 1960. ["Acetonemic vomiting"].. https://pubmed.ncbi.nlm.nih.gov/13804284/
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OBJECTIVE: To estimate renal function and lipid metabolism in pregnant renal transplant recipients. STUDY DESIGN: The study covered 64 women during the third trimester of pregnancy including 33 renal transplant recipients (the study group) and 31 healthy women (the control group). Serum concentrations of uric acid, urea, creatinine, electrolytes, total protein, albumin, acid-base balance and blood cell count were examined to assess renal function. Moreover, the levels of the following lipid metabolism parameters were estimated: (1) total lipids (TL), (2) total LDL fraction (TLDL), (3) total cholesterol (TCh), (4) free cholesterol (fCh), (5) free/total cholesterol (fCh/TCh) ratio, (6) phospholipids (PhL), (7) total cholesterol/phospholipids (fCh/PhL) ratio, (8) triglycerides (TG), (9) HDL-cholesterol (HDL-Ch), (10) LDL-cholesterol (LDL-Ch) and (11) LDL-Ch/HDL-Ch ratio. 'The effect of immunosuppressants (cyclosporine, prednisone and azathioprine) on serum lipid levels was estimated in the study group. The mean maternal age, gestational age and BMI did not differ in both groups. RESULTS: Pregnant renal transplant recipients presented mild renal insufficiency during the third trimester resulting in the increase in serum level of uric acid (P<0.001), urea (P<0.001), creatinine (P<0.001), and Cl- (P<0.001). Proteinuria (1.19+/-1.9 g/24 h) leading to hypoproteinemia (P<0.001) and hypoalbuminemia (P<0.05) confirmed renal function impairment in the study group. Additionally, the diagnosis of renal insufficiency was supported by mild acidosis reflected by a drop in pH (P<0.001). standard HCO3- (P<0.001) and base excess (P<0.001). The women with renal grafts presented vital lipid metabolism disturbances illustrated by the elevated levels of: (1) TL by 72% (P<0.001), (2) TLDL by 21% (P<0.001), (3) TCh by 16% (P<0.001), (4) fCh by 34% (P<0.001), (5) fCh/TCh ratio by 21% (P<0.001), (6) PhL by 28% (P<0.001), (7) TG by 53% (P<0.001), (8) LDL-Ch by 13% (P<0.05) and (9) LDL-Ch/HDL-Ch ratio by 23% (P<0.001). No difference in HDL-Ch level between the two groups was found. Hyperlipidemia in pregnant kidney recipients was associated with immunosuppressive treatment and depended on cyclosporine treatment regimen. Treatment with azathioprine and prednisone was associated with elevated serum levels of examined lipids. CONCLUSION: Serum lipid abnormalities are significantly influenced by the administered dosages of immunosuppressants.
Chronic acidosis is a stimulus for proteolysis in muscle in vivo, but the mechanism of this response is unknown. We tested the hypothesis that acidosis or TNF-alpha, a cytokine whose production increases in acidosis, regulates proteolysis by inhibiting insulin signaling through phosphoinositide 3-kinase (PI3K). In cultured L6 myotubes, acidified (pH 7.1) media did not accelerate the basal protein degradation rate, but it inhibited insulin's ability to suppress proteolysis. Insulin receptor substrate-1 (IRS-1)-associated PI3K activity was not altered in cells acidified for 10 min but was strongly inhibited in cells incubated at pH 7.1 for 24 h. Phosphorylation of Akt was also suppressed by acidification for 24 h. Acidification did not induce changes in IRS-1 abundance, insulin-stimulated IRS-1 tyrosine phosphorylation, or the amount of PI3K p85 regulatory subunit. In contrast to acidification, TNF-alpha suppressed proteolysis in the presence or absence of insulin but had no effect on IRS-1-associated PI3K activity. To establish that the PI3K pathway can regulate protein degradation in muscle, we measured proteolysis in cells after inhibition of PI3K activity with LY-294002 or infection with an adenovirus encoding a dominant negative PI3K p85alpha-subunit. Both approaches inhibited insulin-induced suppression of proteolysis to a degree similar to that seen with acidification. We conclude that acidosis accelerates protein degradation by impairing insulin signaling through PI3K in muscle cells.
In vitro experimental models designed to study the effects of hypoxia and ischemia typically employ oxygen-depleted media and/or hypoxic chambers. These approaches, however, allow for metabolites to diffuse away into a large volume and may not replicate the high local concentrations that occur in ischemic myocardium in vivo. We describe herein a novel and simple method for creating regional hypoxic and ischemic conditions in neonatal rat cardiac myocyte monolayers. This method consists of creating a localized diffusion barrier by placing a glass coverslip over a portion of the monolayer. The coverslip restricts covered myocytes to a thin film of media while leaving uncovered myocytes free to access the surrounding bulk media volume. Myocytes under the coverslip undergo marked morphology changes over time as assessed by video microscopy. Fluorescence microscopy shows that these changes are accompanied by alterations in mitochondrial membrane potential and plasma membrane dynamics and eventually result in myocyte death. We also show that the metabolic activity of myocytes drives cell necrosis under the coverslip. In addition, the intracellular pH of synchronously contracting myocytes under the coverslip drops rapidly, which further implicates metabolic activity in regulating cell death under the coverslip. In contrast with existing models of hypoxia/ischemia, this technique provides a simple and effective way to create hypoxic/ischemic conditions in vitro. Moreover, we conclude that myocyte death is hastened by the combination of hypoxia, metabolites, and acidosis and is facilitated by a reduction in media volume, which may better represent ischemic conditions in vivo.