Effects of coca chewing on the glucose tolerance test
Galarza Guzman M; Penaloza Imana R; Echalar Afcha L; Aguilar Valerio M; Spielvogel H; Sauvain M
Laboratorio de Bioquimica, Instituto Boliviano de Biologia de la Altura, Facultad de Medicina, Universidad Mayor de San Andres, Orstom, Bolivia.
Medicina (B Aires) (Argentina) 1997, 57 (3) p261-4
The effects of coca chewing on the glucose tolerance test were measured. The subjects were 14 habitual coca chewers and 14 non-chewers. All were of Aymara ancestry and came from a rural community from the "Altiplano" close to the city of La Paz. The coca users chewed coca leaves during 3 1/2 hours of the test. The non-chewers showed a significant hypoglycemia at 120 minutes of the test. This effect was not observed in the coca chewers. The hormonal counter-regulation response to hypoglycemia worked perfectly in non-chewers, since glucose levels reached normal values at 180 minutes of the test. These results suggest that coca chewers, at high altitude do not present hypoglycemia, due to an antagonic action of coca metabolites on insulin; allowing a greater availability of glucose in the organism. This would have a positive effect on metabolism in an environment of hypobaric hypoxia, known to lead to situations of hypoglycemia.
Effect of melatonin on hypoglycemia and metoclopramide-stimulated arginine vasopressin secretion in normal men.
Coiro V; Volpi R; Caffarri G; Capretti L; Marchesi C; Giacalone G; Chiodera P
Department of Internal Medicine, School of Medicine, University of Parma, Italy.
Neuropeptides (Scotland) Aug 1997, 31 (4) p323-6
The present study was performed in order to establish whether melatonin (MEL) plays a role in the regulation of arginine vasopressin secretion (AVP) in normal human subjects. For this purpose, the effects of an oral administration of 6 or 12 mg MEL on basal and metoclopramide (MCP)- or hypoglycemia -stimulated AVP secretion was tested in 18 normal men. MCP was given at a dose of 20 mg as an intravenous (i.v.) bolus; hypoglycemia was induced with an i.v. bolus injection of 0.15 IU/kg body weight of insulin. In addition, in view of the well-known inhibitory effect of MEL on the growth hormone (GH) response to hypoglycemia, GH levels were measured during the insulin tolerance test (ITT), as an independent index of MEL activity. MEL did not produce any change in AVP secretory patterns in basal conditions or during the MCP test. In contrast, the mean peak AVP response to hypoglycemia was 2.33 times higher than baseline in the control ITT, whereas it was only 1.77 times higher than baseline in the ITT plus MEL tests. Also, the GH response to hypoglycemia was significantly lower in the presence than in the absence of MEL. For both AVP and GH, the inhibitory effect of MEL during ITT was similar, when either 6 or 12 mg MEL was given. These data indicate an involvement of MEL in the control of the AVP response to hypoglycemia, but not of basal and MCP-induced AVP secretion. In addition, the similar effects of MEL on GH and AVP secretions during ITT suggest that similar neuroendocrine mechanisms underlie these hormonal responses to hypoglycemia.
Oral administration of growth hormone (GH) releasing peptide-mimetic MK-677 stimulates the GH/insulin-like growth factor-I axis in selected GH-deficient adults.
Chapman IM; Pescovitz OH; Murphy G; Treep T; Cerchio KA; Krupa D; Gertz B; Polvino WJ; Skiles EH; Pezzoli SS; Thorner MO
Department of Medicine, University of Virginia, Charlottesville 22908, USA.
J Clin Endocrinol Metab (United States) Oct 1997, 82 (10) p3455-63
To determine the effect of the GH releasing peptide (GHRP)-mimetic, MK-677, on the GH/insulin-like growth factor-I (IGF-I) axis in selected GH-deficient adults, we studied nine severely GH-deficient men [peak serum GH concentration in response to insulin-induced hypoglycemia of 1.2 +/- 1.5 micrograms/L, mean +/- SD (range 0.02-4.79)], age 17-34 yr, height 168 +/- 1.5 cm, body mass index 22.6 +/- 3.3 kg/m2, who had been treated for GH deficiency with GH during childhood. In a double-blind rising-dose design, subjects received once daily oral doses of 10 or 50 mg MK-677 or placebo for 4 days over two treatment periods separated by at least 28 days. Four subjects received placebo and 10 mg/day MK-677 in a cross-over fashion in periods 1 and 2. Five subjects received 10 mg and then 50 mg/day MK-677 in a sequential, rising-dose fashion in periods 1 and 2, respectively. Blood was collected every 20 min for 24 h before treatment and at the end of each period for GH measurement using an ultrasensitive assay. The drug was generally well tolerated, with no significant changes from baseline in circulating concentrations of cortisol, PRL, and thyroid hormones. Serum IGF-i and 24-H mean GH concentrations increased in all subjects after treatment with both 10 and 50 mg/day MK-677 vs. baseline. After treatment with 10 mg MK-677, IGF-I concentrations increased 52 +/- 20% (65 +/- 6 to 99 +/- 9 micrograms/L, geometric mean +/- intrasubject SE, P < or = 0.05 vs. baseline), and 24 h mean GH concentrations increased 79 +/- 19% (0.14 +/- 0.01 to 0.26 +/- 0.02 microgram/L, P < or = 0.05 vs. baseline). Following treatment with 50 mg MK-677, IGF-I concentrations increased 79 +/- 9% (84 +/- 3 to 150 +/- 6 micrograms/L, P < or = 0.05 vs. baseline) and 24-h mean GH concentrations increased 82 +/- 29% (0.21 +/- 0.02 to 0.39 +/- 0.04 microgram/L, P < or = 0.05 vs. baseline), respectively. Serum IGF binding protein-3 concentrations increased with both 10 mg (1.2 +/- 0.1 to 1.7 +/- 0.1 micrograms/L, P < or = 0.05) and 50 mg MK-677 (1.7 +/- 0.1 to 2.2 +/- 0.2 micrograms/L, P < or = 0.05). The GH response to MK-677 was greater in subjects who were the least GH/IGF-I deficient at baseline; by linear regression analysis the increase in 24-h mean GH concentration was positively related to both baseline 24-h mean GH concentration (r = 0.81, P = 0.009) and baseline IGF-I (r = 0.79, P = 0.01) for 10 mg MK-677. IGF-I responses were not significantly related to any baseline measurement. Fasting and postprandial insulin and postprandial glucose increased significantly after MK-677 treatment, and the clinical significance of these changes will need to be assessed in longer term studies. Oral administration of such GHRP-mimetic compounds may have a role in the treatment of GH deficiency of childhood onset.
Alterations in circulating fatty acids and the compartmentation of selected metabolites in women with breast cancer.
Quevedo-Coli S; Crespi C; Benito E; Palou A; Roca P
Departament de Biologia Fonamental i Ciencies de la Salut, Universitat de les Illes Balears, Palma de Mallorca, Spain.
Biochem Mol Biol Int (Australia) Jan 1997, 41 (1) p1-10
The presence of the tumor in women with breast cancer provokes a profile of biochemical change characterized by hypoglycemia, hyperuremia and high levels of free fatty acids and ketone bodies in plasma. The total circulating levels of amino acids and lactate are slightly higher in patients with breast cancer. Moreover, alterations in the circulating levels of free and total fatty acids are associated with enhanced levels of total free fatty acids and significantly lower levels of esterified arachidonic acid. This profile may indicate a state of moderate catabolic activation in breast cancer patients and may also be associated with a slight mobilization of proteins and fatty acids by some of the peripheral tissues in order to cover the needs of the host and the tumor. However, the alteration in the distribution of different fatty acids (saturated, mono-unsaturated and poly-unsaturated) and the different behaviour of the free and esterified fractions may be the result of a greater release of only specific fatty acids by tumor or other host tissues, rather than a higher release of the whole spectrum of free fatty acids. Thus, it is proposed that some of the alterations may be directly related to localized tumor activity.
Nutritional strategies to minimize fatigue during prolonged exercise: fluid, electrolyte and energy replacement.
Dennis SC; Noakes TD; Hawley JA
MRC/UCT Bioenergetics of Exercise Research Unit, University of Cape Town Medical School, Sports Science, Institute of South Africa, Newlands, South Africa.
J Sports Sci (England) Jun 1997, 15 (3) p305-13
While the presence of palatable (20 mmol l-1) concentrations of NaCl in drinks containing carbohydrate consumed during intense exercise would not be expected to promote absorption or significantly help maintain fluid balance, there is no doubt that athletes should ingest some from of carbohydrate (other than fructose) during moderate-intensity exercise lasting > 90 min. As only approximately 20 g of ingested carbohydrate is oxidized in the first hour of exercise, athletes should probably consume 100 ml every 10 min of a dilute (3-5 g 100 ml-1) carbohydrate solution and thereafter increase the carbohydrate concentration to approximately 10 g 100 ml-1 to match the peak (approximately 1 g min-1) rates of plasma glucose oxidation. Drinking more than those amounts of carbohydrate may increase muscle glycogen oxidation by attenuating the fall in plasma insulin concentration and thereby delaying fat mobilization, especially at relatively low (55% of peak oxygen consumption) intensity exercise. As carbohydrate ingestion does not slow the rate of glycogen utilization in working muscle, it is also advisable for endurance athletes to start exercise with an adequate supply of muscle glycogen, irrespective of whether or not they ingest carbohydrate during exercise. While carbohydrate ingestion 'spares' conversion of liver glycogen to plasma glucose and prevents hypoglycemia, it does not delay the fatigue associated with a low (approximately 20 mmol kg-1) glycogen content in working muscle. Conversely, increases in glycogen content of working muscle at the start of exercise have no effect on the rates of plasma glucose oxidation. Higher initial rates of glycogen utilization by active muscles in 'carbohydrate-loaded' subjects decrease the indirect oxidation (via lactate) of non-working muscle glycogen, rather than the conversion of liver glycogen to plasma glucose. Hence, athletes should ingest carbohydrate during endurance exercise even if they have 'carbohydrate-loaded' before exercise.
Metabolic response to lactitol and xylitol in healthy men.
Natah SS; Hussien KR; Tuominen JA; Koivisto VA
Helsinki University Central Hospital, Department of Medicine, Finland.
Am J Clin Nutr (United States) Apr 1997, 65 (4) p947-50
Sugar alcohols are used in food products, yet their metabolic effects in humans are poorly known. We examined plasma glucose, insulin, and C-peptide responses and changes in carbohydrate and lipid oxidation after the ingestion of 25 g lactitol, xylitol, or glucose. Eight healthy, nonobese men were studied after an overnight fast. After the ingestion of lactitol or xylitol, the rise in plasma glucose, insulin, and C-peptide concentrations was less than after the ingestion of glucose (P < 0.02), with no difference between the two polyols. With the glycemic index of glucose as 100, the indexes of xylitol and lactitol were 7 and -1, respectively. A reactive hypoglycemia was observed 3 h after glucose ingestion, but not after the ingestion of sugar alcohols. There were no significant changes in the carbohydrate or lipid oxidation as determined by indirect calorimetry after the ingestion of sugar alcohols. After glucose ingestion, the rise in carbohydrate oxidation was nearly significant (P = 0.07). In conclusion, lactitol and xylitol cause smaller changes than does glucose in plasma glucose and insulin concentrations and thermogenic response. A small hormonal response and the lack of a thermogenic effect may be beneficial when these sugar alcohols are used in food products. The small glucose and insulin responses also suggest that lactitol and xylitol are suitable components of the diet for diabetic patients.
A metabolic complications of nutritional support. I. Carbohydrates, amino acids, fats, water, ions, trace elements
Dr. A. Kazda, Addeleni Klinicke Biochemie, VFN, I Lekarska Fak., Univ Karlova, Karlovo nam. 32, 121 11 Praha 2 Czech Republic
Klinicka Biochemie a Metabolismus (Czech Republic) 1997, 5/4 (251-257)
The paper discusses the metabolic complications described in relation to intake of carbohydrates, amino acids and fats as compounds is parenteral nutrition (PN). Also, the symptoms of possible deficiencies of these nutrients during PN are mentioned. Attention is paid to the dysbalances of selected ions, above all magnesium and phosphate. The significance of trace elements in nutritional support is particularly stressed with respect to metabolism of free radicals. The laboratory monitoring of zinc, and selenium, clinical signs of their deficiency and supplementation during PN are presented. Intoxications described during parenteral supplementation of chromium and manganese are described.
R. Paul St. Amand, M.D., Assistant Clinical Professor of Medicine Endocrinology
U.C.L.A., 4560 Admiralty Way, Suite 355, Marina del Rey, CA 90292
Nutrition almanac/Nutrition Search, Inc. - 3rd ed.
John D. Kirschmann, Director; Lavon J. Dunne,
New York, NY
McGraw-Hill, Publishers Copyright 1990, p.182-3
Hypoglycemia Association, Inc (HAI)
Ashton, MD 20861-0165
Protective effects of pyridoxal phosphate against glucosedeprivation- induced damage in cultured hippocampal neurons
Geng M.-Y.; Saito H.; Nishiyama N.
Dr. N. Nishiyama, Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113 Japan
Journal of Neurochemistry (USA), 1997, 68/6 (2500-2506)
When hippocampal cultures were deprived of glucose, massive release of lactate dehydrogenase (LDH), an indicator of neuronal death, occurred via NMDA receptor activation. Addition of pyridoxal phosphate (PLP; 1 and 10 microM) inhibited this LDH release in a concentration-dependent manner. Prior exposure to PLP evoked more potent inhibitory effects on LDH release compared with those treated at the onset of glucose deprivation. Furthermore, PLP inhibited the reduction of intracellular content of pyruvate induced by glucose deprivation, which was accompanied by the reversal of intracellular ATP depletion. A noteworthy elevation of extracellular glutamate in response to glucose deprivation was completely reversed by addition of PLP. Aminooxyacetic acid, a potent inhibitor of PLP-dependent enzymes, antagonized the effects of PLP on LDH release, pyruvate production, and ATP formation. These results suggest that PLP protects neurons from glucose deprivation- induced damage by enhancing the formation of energy-yielding products and relieving extracellular load of glutamate. The observed phenomena further indicate that PLP might be used prophylactically against neuronal death induced by metabolic disorders.
Chromium and other insulin sensitizers may enhance glucagon secretion: Implications for hypoglycemia and weight control
Nutrition 21, Suite 335, 1010 Turquoise Street, San Diego, CA 92109 USA
Medical Hypotheses (United Kingdom), 1996, 46/2 (77-80)
Increased pancreatic beta-cell secretory activity usually is associated with decreased alpha-cell activity; stimulated beta-cells release gamma-aminobutyric acid, which hyperpolarizes alpha-cells, inhibiting glucagon release. Thus, insulin secretion and glucagon secretion are usually inversely coupled. This suggests that chromium and other insulin-sensitizing modalities, by down-regulating beta-cell activity, may increase glucagon secretion. Such an effect might play a role in the documented therapeutic activity of supplemental chromium and biguanides in reactive hypoglycemia, and might also be of benefit to dieters.
Durk Pearson and Sandy Shaw
Anti-Aging News, January 1982 Vo.2, No. 1 pg 6-7
Cysteine is a strong reducing agent (it can prevent oxidation of some other substances). In fact, it has been found that too much cysteine in a cell culture medium can inactivate the hormone insulin contained in the medium. The insulin molecule contains three disulfide bonds, at least one of which can be reduced by cysteine. When this happens, the insulin molecule can no longer maintain the proper shape to function normally in stimulating the metabolism of sugar. In hypoglycemia attacks, there is too much insulin and too little sugar in the blood stream. Cysteine can inactivate insulin, thereby allowing the sugar level to begin to rise again. We and others have used the combination of vitamins B1, C, and cysteine to successfully abort severe attacks of hypoglycemia. A reasonable dose for a healthy adult is 5 grams of C, 1 gram of B1, and 1 gram cysteine. Although cysteine is a nutrient, it s use on a long-term basis should be considered experimental. Start with a low dose (250 milligrams per day) and work your way up. Always use at least three times as much Vitamin-C as cysteine. Be sure to consult with your physician and have regular clinical tests of basic body functions, especially liver and kidney. Diabetics should not use cysteine supplements due to its anti-insulin effects.
Glutathione protects against hypoxic/hypoglycemic decreases in 2-deoxyglucose uptake and presynaptic spikes in hippocampal slices.
Shibata S; Tominaga K; Watanabe S
Department of Pharmacology, Faculty of Pharmaceutical Sciences, Kyushu University, Fukuoka, Japan.
Eur J Pharmacol (Netherlands) Jan 24 1995, 273 (1-2) p191-5
The effects of glutathione, its analogue: YM737 (N-(N-gamma-L-glutamyl-L- cysteinyl) glycine l-isopropyl ester sulfate monohydrate), a monoester of glutathione, and N-acetyl-L-cysteine on hypoxia/hypoglycemia-induced decreases in CA1 presynaptic fiber spikes and 2-deoxyglucose uptake were investigated using rat hippocampal slices. The drugs were added to normal medium for 30 min before the incubation under hypoxic/hypoglycemic conditions (20 min), and, after a 3-h washout, presynaptic potential or 2-deoxyglucose uptake in hippocampal slices was measured. Treatment with glutathione, YM737 and N-acetyl-L-cysteine produced an attenuation of the hypoxia/hypoglycemia-induced decrease in presynaptic fiber spikes and 2-deoxyglucose uptake. The order of potency for neuroprotective action was YM737 > or = N-acetyl-L-cysteine > glutathione. The present results suggest a role for glutathione in improving hypoxia/hypoglycemia-induced dysfunction of hippocampal regions.