Kinetic Determination of Serum Glucose by Use of the Hexokinase/Glucose-6-phosphate Dehydrogenase Method

Deeg, R.; Kraemer, W J; Ziegenhorn, Joachim

doi:10.1515/cclm.1980.18.1.49

Cited by 22 publications

(19 citation statements)

References 3 publications

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“…Amastigote burdens in the splenic aspirates were graded on a logarithmic scale, from 0 (no amastigotes in 1000 microscopic fields) to 6 (.100 amastigotes/microscropic field) (Chulay and Bryceson, 1983). Serum concentrations of total cholesterol were determined (again, as part of the routine investigation), in a Microlab-200 chemistry analyser (Merck, Darmstadt, Germany), using a commercial enzymatic colorimetric assay (Merck Diagnostic, Mumbai, India) based on the 'CHOD-PAP' method (Deeg and Ziegenhorn, 1983).…”

Section: Methodsmentioning

confidence: 99%

Human visceral leishmaniasis: decrease in serum cholesterol as a function of splenic parasite load

Ghosh

Lal²,

Pandey³

et al. 2011

Annals of Tropical Medicine & Parasitology

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Section: Methodsmentioning

confidence: 99%

Human visceral leishmaniasis: decrease in serum cholesterol as a function of splenic parasite load

Ghosh

Lal²,

Pandey³

et al. 2011

Annals of Tropical Medicine & Parasitology

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“…Plasma TAG concentration was determined by enzymatic methods (44). Plasma glucose concentrations was analyzed by standard enzymatic methods (10). Plasma insulin, total GIP, total glucagon-like peptide (GLP)-1, and intact GLP-2 concentrations were measured by radioimmunoassay as previously described (1,9,23,25).…”

Section: Blood Analysismentioning

confidence: 99%

On the role of glucose-dependent insulintropic polypeptide in postprandial metabolism in humans

Asmar

Tangaa

Madsbad

et al. 2010

American Journal of Physiology-Endocrinology and Metabolism

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(GIP) in the regulation of gastric emptying (GE), appetite, energy intake (EI), energy expenditure (EE), plasma levels of triglycerides (TAG), and free fatty acids (FFA) in humans. First, 20 healthy males received intravenous infusion of GIP (0.8 pmol · kg Ϫ1 · min Ϫ1 ) or saline for 300 min during and after a fixed meal (protocol 1). GE was measured using paracetamol, appetite sensations using visual analog scales, EE using indirect calorimetry, and EI during a subsequent ad libitum meal (at 300 min). Next, 10 healthy males received intravenous infusions of Intralipid, glucose, or Intralipid plus glucose, with and without GIP (1.5 pmol · kg Ϫ1 · min Ϫ1 ) for 300 min (protocol 2). In protocol 1, GIP did not have any effect on GE, EI, EE, removal of TAG, or FFA and did not influence the subjective feeling of hunger, satiety, fullness or prospective food consumption compared with saline. In protocol 2, no difference was seen in the plasma TAG on Intralipid ϩ GIP/saline and Intralipid ϩ glucose ϩ GIP/saline days. FFA concentrations were lower on Intralipid ϩ glucose ϩ GIP/saline days (P Ͻ 0.05) compared with Intralipid ϩ GIP/saline days and on Intralipid ϩ GIP day (P Ͻ 0.004) compared with Intralipid ϩ saline day. Insulin increased on all GIP days compared with saline days (P Ͻ 0.05). In conclusion, while confirming its insulinotropic effects, these data suggest that GIP does not affect GE, appetite, energy intake, EE, or the clearance rate of the applied TAG formulation in humans. However, both insulin and GIP lower post-Intralipid FFA concentration, GIP probably via stimulation of insulin secretion, increasing FFA reesterification. gastric emptying; energy intake; energy expenditure; appetite; insulin OBESITY IS A CONSEQUENCE of an imbalance between food intake and energy expenditure, and several lines of evidence suggest a role for glucose-dependent insulinotropic polypeptide (GIP) in the development of obesity. GIP is a hormone secreted from endocrine K cells located in the proximal part of the small intestine in connection with food intake (18,31,38), and it stimulates insulin secretion in a glucose-dependent manner (2,11,36). Early observations of elevated plasma GIP concentrations in type 2 diabetic patients (8,12,14,43) and obese diabetic ob/ob mice (21) drew attention to a possible role of GIP in fat metabolism. This is supported by studies (3) demonstrating that high-fat feeding induced K-cell hyperplasia and enhanced GIP gene expression. Furthermore, it has been shown that GIP is released by lipids and that 24-h GIP profiles parallel the plasma concentration of triglycerides (TAG; Ref. 15), leading to speculation that GIP might play a part in the postprandial regulation of TAG. In dogs, infusion of GIP significantly lowered the rise in plasma TAG after infusion of chylomicrons (45), while in rats exogenous and endogenous GIP lowered the plasma TAG response to a fat load (13). In adipose tissue, GIP has been shown to stimulate glucose transport and increase fatty acid synthesis (24), enhance lipoprotein...

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“…24 Blood for glucose and lactate were collected in EDTAtubes prepared with¯ouride, and plasma analysed by standard enzymatic methods. 25,26 For hormone analysis the syringes contained EDTA (6 mmolal) and aprotinin (500 kIUal, ®nal concentrations), and after centrifugation, plasma was kept frozen at À20 C. Insulin concentrations in plasma were measured against standards of human insulin by radioimmunoassay (RIA) according to the principles described by Albano et al 27 The tracer was human insulin, monoiodinated in positon A14 (a gift from Novo Nordisk AaS, Bagsvaerd, Denmark). The glucagon RIA was directed against the carboxy terminus of the glucagon molecule (antibody code 4305).…”

Section: Rmr Kjmentioning

confidence: 99%

The effect of physiological levels of glucagon-like peptide-1 on appetite, gastric emptying, energy and substrate metabolism in obesity

Flint¹,

Raben²,

Ersbøll³

et al. 2001

Int J Obes

319

228

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OBJECTIVE: Peripheral infusions of glucagon-like peptide-1 (GLP-1) in humans have been shown to inhibit gastrointestinal motility and decrease hunger and energy intake. However, these investigations used supraphysiological doses. The objective of this study was to investigate the effects of a GLP-1 infusion in a physiological dose on appetite sensations, energy intake, gastric emptying, energy and substrate metabolism. METHODS: Eighteen obese men participated in the placebo-controlled, randomized, single-blinded, cross-over study with infusion of GLP-1 or saline. Resting metabolic rate (RMR) and substrate oxidations were measured by ventilated hood before and after an energy-®xed breakfast. Gastric emptying was measured using paracetamol as a marker. Visual analogue scales were used to assess appetite sensations, thirst and comfort throughout the experiment and palatability of the test meals. Blood was sampled for analysis of hormones (GLP-1, GLP-2, glucose-dependent insulinotropic polypeptide (GIP), insulin, glucagon), and substrates (glucose, lactate, non-esteri®ed fatty acids (NEFA), triacylglycerol (TAG)). Ad libitum energy intake at lunch was registered. RESULTS: Following the breakfast, GLP-1 infusion suppressed ratings of hunger and prospective food consumption (P`0.05), whereas all other subjective ratings and ad libitum energy intake were unaffected. RMR, carbohydrate oxidation and gastric emptying rate were lower during the GLP-1 infusion compared with the saline infusion (P`0.001, P`0.05, P`0.0001, respectively). All plasma hormone and substrate pro®les, except NEFA, were signi®cantly reduced by GLP-1 (P`0.0001). CONCLUSION: It is concluded that GLP-1 in physiological concentrations powerfully reduces the rate of entry of nutrients into the circulation by a reduction of gastric emptying rate in obese subjects. The effect of GLP-1 on appetite and food intake may be bene®cial in weight reduction.

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Kinetic Determination of Serum Glucose by Use of the Hexokinase/Glucose-6-phosphate Dehydrogenase Method

Cited by 22 publications

References 3 publications

Human visceral leishmaniasis: decrease in serum cholesterol as a function of splenic parasite load

Human visceral leishmaniasis: decrease in serum cholesterol as a function of splenic parasite load

On the role of glucose-dependent insulintropic polypeptide in postprandial metabolism in humans

The effect of physiological levels of glucagon-like peptide-1 on appetite, gastric emptying, energy and substrate metabolism in obesity

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