sodium-bicarbonate and Obesity

Late-night supper increases the risk of postprandial reflux from the acid pocket especially in obesity. An alginate-based, raft-forming medication may be useful for obese patients with GERD.. To compare the efficacy of Gaviscon Advance (Reckitt Benckiser, UK) and a non-alginate antacid in post-supper suppression of the acid pocket and post-prandial reflux among obese participants.. Participants underwent 48 h wireless and probe-based pH-metry recording of the acid pocket and lower oesophagus, respectively, and were randomised to single post-supper (10 pm) dose of either Gaviscon Advance or a non-alginate antacid on the second night. Primary outcomes were suppression of median pH of acid pocket and lower oesophagus, measured every 10-minutes post-supper for 1 h. Secondary outcomes were suppression of % time pH < 4 at lower oesophagus and improvement in frequency and visual analogue score (VAS) of regurgitation.. Of the 81 screened participants, 55 were excluded and 26 (mean age 33.5 years, males 77.8% and BMI 32.8 kg/m. Among obese individuals, Gaviscon Advance was superior to a non-alginate antacid in post-supper suppression of the acid pocket. (Clinical trial registration unique identifier: NCT03516188).

Topics: Adult; Alginates; Aluminum Hydroxide; Antacids; Anti-Ulcer Agents; Drug Combinations; Female; Gastric Acid; Gastroesophageal Reflux; Humans; Hydrogen-Ion Concentration; Malaysia; Male; Meals; Middle Aged; Obesity; Postprandial Period; Silicic Acid; Sodium Bicarbonate; Time Factors; Treatment Outcome; Young Adult

The aim of this study was to evaluate the use of the [14C]-sodium bicarbonate/urea technique to measure the change in total energy expenditure after weight loss and a period of weight maintenance. Eleven healthy subjects (6 men and 5 women aged 50 +/- 3 yrs, BMI 34.1 +/-2.1 kg/ m2, body fat 38.7 +/-3%) underwent 8 weeks of energy restriction using a combination of "Modifast" formula and one small meal per day (approximately 3.3 MJ/day). For an additional 2 weeks, subjects resumed a solid food diet that contained enough energy to stabilize body weight at the newly reduced level. Body composition, total energy expenditure (TEE), resting energy expenditure (REE) and the thermic effect of a 2.7 MJ test meal (TEF) were measured at both weeks 0 and 10. At week 10 as compared to week 0, body weight decreased by 12.2+/-1.6 kg (12.5%)(P<0.001). Total fat and lean mass decreased by 8.4+/-1.0 kg (20.4%) and 3.8+/-0.7 kg (6.7%), respectively (P< 0.001). REE decreased by 500+/-128 kJ/day (5.6+/-1.3%)(P<0.002). Decreases in the TEE (0.18 +/-;3.7%)and TEF(1.4+/-0.9%) were not significant. In conclusion, although [14C]-sodium bicarbonate/urea was well tolerated and did not interfere with normal daily activities, it did not have sufficient sensitivity to accurately measure weight loss induced changes in TEE in the range of 0.1-10%.

Topics: Adult; Body Composition; Body Mass Index; Carbon Radioisotopes; Creatinine; Diet, Reducing; Energy Intake; Energy Metabolism; Female; Food; Food, Formulated; Humans; Male; Middle Aged; Obesity; Sodium Bicarbonate; Urea; Weight Loss

Impairments in insulin sensitivity can occur in patients with chronic kidney disease (CKD). Correction of metabolic acidosis has been associated with improved insulin sensitivity in CKD, suggesting that metabolic acidosis may directly promote insulin resistance. Despite this, the effect of acid or alkali loading on insulin sensitivity in a rodent model of CKD (remnant kidney) has not been directly investigated. Such studies could better define the relationship between blood pH and insulin sensitivity. We hypothesized that in remnant kidney rats, acid or alkali loading would promote loss of pH homeostasis and consequently decrease insulin sensitivity. To test this hypothesis, we determined the impact of alkali (2 wk) or acid (5-7 days) loading on plasma electrolytes, acid-base balance, and insulin sensitivity in either sham control rats, 2/3 nephrectomized rats, or 5/6 nephrectomized rats. Rats with 5/6 nephrectomy had the greatest response to insulin followed by rats with 2/3 nephrectomy and sham control rats. We found that treatment with 0.1 M sodium bicarbonate solution in drinking water had no effect on insulin sensitivity. Acid loading with 0.1 M ammonium chloride resulted in significant reductions in pH and plasma bicarbonate. However, acidosis did not significantly impair insulin sensitivity. Similar effects were observed in Zucker obese rats with 5/6 nephrectomy. The effect of renal mass reduction on insulin sensitivity could not be explained by reduced insulin clearance or increased plasma insulin levels. We found that renal mass reduction alone increases sensitivity to exogenous insulin in rats and that this is not acutely reversed by the development of acidosis.

Topics: Acid-Base Equilibrium; Animals; Creatinine; Glucose Tolerance Test; Insulin; Insulin Resistance; Kidney; Nephrectomy; Obesity; Organ Size; Rats; Rats, Sprague-Dawley; Rats, Zucker; Renal Insufficiency, Chronic; Sodium Bicarbonate; Sodium Chloride

Topics: Alginates; Aluminum Hydroxide; Antacids; Drug Combinations; Esophagitis, Peptic; Gastroesophageal Reflux; Humans; Obesity; Silicic Acid; Sodium Bicarbonate

Topics: Alginates; Aluminum Hydroxide; Antacids; Drug Combinations; Esophagitis, Peptic; Gastroesophageal Reflux; Humans; Obesity; Silicic Acid; Sodium Bicarbonate

This study evaluated the effects of oral sodium bicarbonate (NaHCO3) supplementation on ammonium (NH4+) nitrogen (N) and urea N excretion and on ketone bodies during the metabolic acidosis of a very low energy protein diet. Ten healthy obese female subjects (BMI, 38.4 +/- 1.5 kg/m2;weight, 100 +/- 4 kg) were given a 1.72 MJ (412 kcal) all protein (16.8 g N) liquid formula, 16 mmol KCl and a multivitamin-mineral supplement daily for 4 weeks. In addition, the five subjects in group 1 received 60 mmol Na+ daily as sodium chloride (NaCl) for 3 weeks and as NaHCO3 during week 4. The subjects in group 2 were given 40 mmol/d NaHCO3 during the first week, 60 mmol/d during weeks 2 and 3, and 60 mmol/d NaCl during week 4. Nitrogen balance was achieved in both groups by the end of week 3. The subjects in group 1 at week 2 showed an increase in blood [H+] of 0.41 +/- 0.06 x 10(-8) mol/L and a decrease in blood bicarbonate from 26.0 +/- 0.8 to 23.8 +/- 1.2 mmol/L. The subsequent NaHCO3 curtailed NH4+ N excretion by one half, without significant change in ketone body levels or excretion. Administration of NaHCO3 from the start of the diet to the subjects in group 2 prevented both the metabolic acidosis and the increase in NH4+ N excretion and attenuated the increase in blood and urine 3-hydroxybutyrate. When NaCl replaced NaHCO3 during week 4, ammonium N excretion doubled. Urea N excretion was comparable in both groups and was unaffected by bicarbonate.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Bicarbonates; Dietary Proteins; Energy Metabolism; Female; Humans; Hydroxybutyrates; Ketone Bodies; Nitrogen; Obesity; Potassium; Sodium; Sodium Bicarbonate; Urea

We have investigated whole body protein turnover in the fasted state in five normal men, five male Type 1 diabetic patients off insulin therapy, and five obese women, using IV 13C-leucine as a tracer. In diabetic patients, there was, as expected, a greater net loss of protein in the fasted state than in normal subjects. However, contrary to animal and studies in vitro, our diabetic patients in the fasted state showed a greater rate of protein synthesis than normal subjects (p less than 0.01). The increased net loss of protein in diabetic patients compared with normal subjects arose because, in the diabetic patients, protein breakdown was increased even more than protein synthesis under the conditions of this study. Plasma leucine concentration was higher in diabetic and in insulin-insensitive obese patients than in normal subjects (p less than 0.01), and higher in diabetic than in obese patients (p less than 0.05). The rate of protein synthesis per kg lean body mass was also higher in diabetic patients than in obese or normal subjects (p less than 0.01), and higher in obese than normal subjects (p less than 0.05). We conclude that, in human subjects, whole body leucine and protein metabolism are very sensitive to the action of insulin.

Topics: Adult; Bicarbonates; Blood Glucose; C-Peptide; Carbon Isotopes; Diabetes Mellitus, Type 1; Female; Humans; Insulin; Leucine; Male; Obesity; Proteins; Reference Values; Sodium Bicarbonate

During a total fast in obese subjects, the daily rate of nitrogen excretion undergoes only a small further decline after 2 wk, the excretion rate being about 5 g N/day. At this time, ammonium and urea each constitute about one-half of this excretion. The purpose of this study was to consider two alternative hypotheses: first, that the near plateau in nitrogen excretion represents an irreducible minimum rate of net protein breakdown in order to supply essential organs with calories in the form of glucose; second, that protein breakdown could be further reduced by minimizing the requirement to provide nitrogen for ammonium excretion during the ketoacidosis of fasting. Because ammonium excretion is largely controlled by acid-base balance, 150 mmol of sodium bicarbonate plus 60 mmol of potassium chloride were administered daily to decrease ammonium excretion in eight obese subjects who were totally fasting for more than 14 days. Urine ammonium nitrogen fell with this treatment (from 3.8 +/- 0.4 to 2.0 +/- 0.4 g N/g creatinine). In addition, there was a smaller fall in the rate of urea excretion (from 2.5 +/- 0.2 to 2.1 +/- 0.3 g N/g creatinine) together with a fall in the blood urea nitrogen. Therefore, it appears that ammonium excretion contributes to the negative nitrogen balance of a prolonged total fast, as assessed over a 3-day period of observation, is responsible for about one-third of the net lean body mass loss.

Topics: Acidosis; Adult; Bicarbonates; Blood Urea Nitrogen; Fasting; Female; Humans; Ketone Bodies; Ketosis; Male; Middle Aged; Nitrogen; Obesity; Potassium Chloride; Proteinuria; Sodium Bicarbonate

Topics: Acidosis; Apnea; Atropine; Bicarbonates; Bis-Trimethylammonium Compounds; Gallamine Triethiodide; Humans; Infusions, Parenteral; Laparotomy; Meperidine; Neostigmine; Nitrous Oxide; Obesity; Peritonitis; Postoperative Complications; Sodium Bicarbonate; Thiopental; Toxicology