oligomycins and Body-Weight

To examine the effect of 50% food restriction over a period of 3 days on mitochondrial energy metabolism, liver mitochondria were isolated from ad libitum and food-restricted rats. Mitochondrial enzyme activities and oxygen consumption were assessed spectrophotometrically and polarographically. With regard to body weight loss (-5%), food restriction decreased the liver to body mass ratio by 7%. Moreover, in food-restricted rats, liver mitochondria displayed diminished state 3 (-30%), state 4-oligomycin (-26%) and uncoupled state (-24%) respiration rates in the presence of succinate. Furthermore, "top-down" elasticity showed that these decreases were due to an inactivation of reactions involved in substrate oxidation. Therefore, it appears that rats not only adapt to food restriction through simple passive mechanisms, such as liver mass loss, but also through decreased mitochondrial energetic metabolism.

Topics: Animals; Body Weight; Citrate (si)-Synthase; Electron Transport Complex IV; Energy Metabolism; Food Deprivation; Membrane Potentials; Mitochondria, Liver; Oligomycins; Organ Size; Oxidoreductases, N-Demethylating; Oxygen Consumption; Rats; Rats, Sprague-Dawley; Succinic Acid; Time Factors

Hepatocytes were isolated from eight species of birds ranging from 13 g zebra finches to 35 kg emus. This represents a 2800-fold range of body mass (Mb). Liver mass (g) was allometrically related to species body mass by the equation: liver mass=19.6 x Mb(0.91). There was a significant allometric decline in hepatocyte respiration rate (HRR; nmol O2 mg(-1) dry mass min(-1)) with species body mass (kg) described by the relationship: HRR=5.27 x Mb(-0.10). The proportions of hepatocyte oxygen consumption devoted to (i) mitochondrial ATP production, (ii) mitochondrial proton leak and (iii) non-mitochondrial processes were estimated by using excess amounts of appropriate inhibitors. It was found that although hepatocyte respiration rate varied with body mass in birds, these processes constitute a relatively constant proportion of hepatocyte metabolic rate irrespective of the size of the bird species. The respective percentages were 54%, 21% and 25%. The portion of hepatocyte respiration devoted to ATP production for use by the sodium pump was estimated and found to be a relatively constant 24% of hepatocyte respiration and 45% of mitochondrial ATP production in different-sized bird species. These results are discussed in the context of competing theories to explain the metabolism-body size allometry, and are found to support the 'allometric cascade' model.

Topics: Adenosine Triphosphate; Animals; Basal Metabolism; Birds; Body Weight; Cell Count; Hepatocytes; Liver; Mitochondria; Models, Biological; Oligomycins; Organ Size; Ouabain; Oxygen Consumption; Sodium-Potassium-Exchanging ATPase

Adaptive increases in renal bicarbonate reabsorption occur in response to acute increases in filtered bicarbonate (FLHCO3). In a previous study, we showed that an increase in FLHCO3 induced by plasma volume expansion increased the Vmax for Na+/H+ exchange activity in renal cortical brush border membrane vesicles (BBMV), providing a potential mechanism for the adaptive increase in HCO3- reabsorption. The present studies were undertaken to determine whether the increase in FLHCO3 induced by plasma expansion also stimulates the other major H+ transporter in cortical BBMV, the H(+)-ATPase. H(+)-ATPase activity was assessed in BBMV obtained from hydropenic and plasma expanded Munich-Wistar rats, using a NADH-linked ATPase assay. H(+)-ATPase activity was measured as the ouabain and oligomycin-insensitive, bafilomycin A1-sensitive component of total ATPase activity. Acute plasma expansion doubled single nephron FLHCO3, and this change was associated with a 64% increase in the Vmax for H(+)-ATPase activity, with no change in apparent Km. The Vmax for H(+)-ATPase activity correlated directly with whole kidney GFR and FLHCO3 (r = 0.68 and 0.72, respectively), and with single nephron GFR and FLHCO3 (r = 0.76 and 0.80, respectively). Thus, the mechanism for the adaptive increase in proximal tubular HCO3- reabsorption that occurs in response to acute increases in FLHCO3 appears to be related to increased activity of both H(+)-ATPase and Na+/H+ exchange in the apical membrane of the proximal tubule epithelium.

Topics: Absorption; Adaptation, Physiological; Adenosine Triphosphate; Animals; Anti-Bacterial Agents; Bicarbonates; Body Weight; Enzyme Inhibitors; Isotonic Solutions; Kidney Tubules, Proximal; Kinetics; Macrolides; Male; Microvilli; Oligomycins; Ouabain; Plasma Substitutes; Proton-Translocating ATPases; Rats; Rats, Wistar; Ringer's Lactate; Sodium-Hydrogen Exchangers; Ultrafiltration

Topics: Adenine Nucleotides; Adenosine Triphosphatases; Aniline Compounds; Animals; Ascorbic Acid; Biological Transport; Body Weight; Calcium; Endoplasmic Reticulum; Female; Malates; Mitochondria, Muscle; Muscles; Muscular Atrophy; Oligomycins; Organ Size; Oxidative Phosphorylation; Oxygen Consumption; Polarography; Pyruvates; Rats; Rotenone; Succinates; Time Factors; Triamcinolone; Triamcinolone Acetonide; Uncoupling Agents