High-Pressure Liquid Chromatographic Analysis of Indocyanine Green

Rappaport, P.L.; Thiessen, Jake J.

doi:10.1002/jps.2600710205

Cited by 56 publications

(41 citation statements)

References 10 publications

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“…Body composition was measured using dual-energy X-ray absorptiometry (DPX scanner; Hologic, Waltham, MA) combined with a computerized tomographic scan at T11-12 and L3-4. Plasma [3-3 H]glucoseϪspecific activity and enrichments of deuterium on the 2nd and 5th carbon of plasma glucose were measured as previously described (18,(22)(23)(24)(25). Calculations.…”

Section: Methodsmentioning

confidence: 99%

Obesity and Type 2 Diabetes Impair Insulin-Induced Suppression of Glycogenolysis as Well as Gluconeogenesis

et al. 2005

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To determine whether the hepatic insulin resistance of obesity and type 2 diabetes is due to impaired insulininduced suppression of glycogenolysis as well as gluconeogenesis, 10 lean nondiabetic, 10 obese nondiabetic, and 11 obese type 2 diabetic subjects were studied after an overnight fast and during a hyperinsulinemic-euglycemic clamp. Gluconeogenesis and glycogenolysis were measured using the deuterated water method. Before the clamp, when glucose and insulin concentrations differed among the three groups, gluconeogenesis was higher in the diabetic than in the obese nondiabetic subjects (P < 0.05) and glycogenolysis was higher in the diabetic than in the lean nondiabetic subjects (P < 0.05). During the clamp, when glucose and insulin concentrations were matched and glucagon concentrations were suppressed, both glycogenolysis and gluconeogenesis were higher (P < 0.01) in the diabetic versus the obese and lean nondiabetic subjects. Furthermore, glycogenolysis and gluconeogenesis were higher (P < 0.01) in the obese than in the lean nondiabetic subjects. Plasma free fatty acid concentrations correlated (P < 0.001) with glucose production and gluconeogenesis both before and during the clamp and with glycogenolysis during the clamp (P < 0.01). We concluded that defects in the regulation of glycogenolysis as well as gluconeogenesis cause hepatic insulin resistance in obese nondiabetic and type 2 diabetic humans. Diabetes 54: [1942][1943][1944][1945][1946][1947][1948] 2005 T ype 2 diabetes is characterized by both fasting and postprandial hyperglycemia. Numerous studies have established that glucose production in people with type 2 diabetes is either elevated or not appropriate for the prevailing glucose and insulin concentrations (1-8). The cause(s) of these inappropriately elevated rates of glucose production remains an area of active investigation. A series of studies have shown that gluconeogenesis, whether measured with magnetic resonance spectroscopy (7) or the deuterated water method, is increased in people with type 2 diabetes (2,9 -13). On the other hand, rates of glycogenolysis have been reported to not differ in diabetic and nondiabetic individuals (2,9,10,12). However, because both hyperglycemia and hyperinsulinemia are potent inhibitors of glycogenolysis (14 -17), equal rates of glycogenolysis, despite higher glucose and insulin concentrations in diabetic subjects, imply abnormal regulation of the glycogenolytic as well as the gluconeogenic pathway.We recently confirmed this supposition (11) by demonstrating that the contribution of glycogenolysis to endogenous glucose production (henceforth referred to as glycogenolysis) was fully suppressed in nondiabetic subjects when insulin concentrations were clamped at levels slightly above basal and glucose concentrations were raised to levels typically observed in people with type 2 diabetes (i.e., ϳ11 mmol/l). In contrast, glycogenolysis persisted in people with mild (e.g., fasting glucose ϳ8 mmol/l) or severe (e.g., fasting glucose ϳ12 mmol/l) diabetes who...

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Section: Methodsmentioning

confidence: 99%

Obesity and Type 2 Diabetes Impair Insulin-Induced Suppression of Glycogenolysis as Well as Gluconeogenesis

et al. 2005

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“…The run time of each injection (50 l) was 20 min. ICG was detected by an Applied Biosystems (Foster City, CA) programmable absorbance detector (785A) with a tungsten lamp set at 700 nm (Rappaport and Thiessen, 1982). The retention time of ICG was approximately 11.0 min.…”

Section: Metabolism Of Rofecoxib In Humansmentioning

confidence: 99%

The Disposition and Metabolism of Rofecoxib, a Potent and Selective Cyclooxygenase-2 Inhibitor, in Human Subjects

Halpin

Porras²,

Geer³

et al. 2002

Drug Metab Dispos

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ABSTRACT:The disposition and metabolism of rofecoxib, a selective cyclooxygenase-2 inhibitor, were examined in healthy human subjects and in cholecystectomy patients. After oral administration of [ 14 C]rofecoxib (125 mg, 100 Ci) to healthy subjects, the mean concentrations of total radioactivity and rofecoxib in plasma as a function of time indicated that the t max was achieved at 9 h postdose. After t max , levels of both radioactivity and rofecoxib decreased in a parallel, exponential fashion (effective t (Prasit et al., 1999), an inducible isoform of cyclooxygenase that plays a key role in inflammatory processes. Rofecoxib has been approved for the treatment of arthritis and pain, and was developed on the premise that selective inhibition of COX-2 would result in decreased inflammation without the adverse gastrointestinal effects associated with inhibition of COX-1 (Vane and Botting, 1996; Donnelly and Hawkey, 1997; Jouzeau et al., 1997). This hypothesis has been supported by the results of recent clinical trials, including the VIGOR study, in which rheumatoid arthritis patients treated with rofecoxib displayed significantly fewer clinically important gastrointestinal events than patients treated with naproxen, a nonselective COX inhibitor (Bombardier et al., 2000).1Disposition and metabolism of rofecoxib in rats and dogs were reported recently (Halpin et al., 2000); metabolites identified in both species included 5-hydroxyrofecoxib, 5-hydroxyrofecoxib-O-␤-Dglucuronide, and trans-3,4-dihydro-rofecoxib, while additional metabolites identified in rat only were cis-3,4-dihydro-rofecoxib, rofecoxib-3Ј,4Ј-dihydrodiol, and 4Ј-hydroxyrofecoxib sulfate. Of note, following oral administration of rofecoxib to intact rats, was the appearance of a second C max which was not observed in bile duct-cannulated rats. This phenomenon was found to be due to a novel form of enterohepatic recycling, which involved reversible metabolism of rofecoxib to 5-hydroxyrofecoxib (Baillie et al., 2001).The studies presented here describe the disposition and metabolism of rofecoxib in human subjects. The specific objectives of these studies were: 1) to examine the absorption and excretion of [ 14 C]rofecoxib in healthy adult volunteers and to compare the results with those obtained from animals, 2) to identify the urinary metabolites of rofecoxib in humans, 3) to examine the extent of conversion of 5-hydroxyrofecoxib to rofecoxib following oral administration of 5-hydroxyrofecoxib to healthy subjects, and 4) to investigate the possible involvement of biliary elimination in the excretion of rofecoxib and its metabolites in humans.

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“…Plasma insulin concentrations were measured by radioimmunoassay (15). Plasma indocyanine green concentrations were measured by a modification of a previously published HPLC technique (16). Briefly, 0.5 ml ofplasma was mixed with 50 ,l ofmethanolic diazepam (1 mg in 100 ml) as the internal standard, and 0.5 ml ofacetonitrile was added to precipitate plasma proteins.…”

Section: Materials [L1-'4c]palmitate (Research Products Internationalmentioning

confidence: 99%

Effects of body fat distribution on regional lipolysis in obesity.

Martin

Jensen²

1991

J. Clin. Invest.

244

166

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High-Pressure Liquid Chromatographic Analysis of Indocyanine Green

Cited by 56 publications

References 10 publications

Obesity and Type 2 Diabetes Impair Insulin-Induced Suppression of Glycogenolysis as Well as Gluconeogenesis

Obesity and Type 2 Diabetes Impair Insulin-Induced Suppression of Glycogenolysis as Well as Gluconeogenesis

The Disposition and Metabolism of Rofecoxib, a Potent and Selective Cyclooxygenase-2 Inhibitor, in Human Subjects

Effects of body fat distribution on regional lipolysis in obesity.

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