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Biomedical subjects

J Maturo

Publications and source records attributed to J Maturo.

9 recordsLinked to original sources
PubMed1993

Modification of insulin resistance by diazoxide in obese Zucker rats.

Hyperinsulinism, insulin resistance, and decreased number of insulin receptors are characteristic of obesity in both humans and experimental animals. To assess the role of insulin in developing obesity, diazoxide (DZ), an inhibitor of glucose-stimulated insulin secretion, was administered for 8 weeks to 7-week-old female Zucker rats in two concentrations, 50 mg/kg.day (LD-DZ), and 100 mg/kg.day (HD-DZ). The obese and lean rats were divided into three subgroups: diazoxide (DZ), pair-fed (PF), and control (C) groups (n = 6 rats/subgroup-genotype). Diazoxide-treated obese and lean animals showed significantly lower postabsorptive plasma insulin concentrations (P < 0.005) than their respective obese and lean PF and C subgroups. HD-DZ obese rats consumed more calories (P < 0.001), yet gained less weight (P < 0.05) than PF and C rats. The plasma glucose concentrations in the postabsorptive state and during glucose tolerance tests in HD-DZ obese rats were significantly lower than those in PF and C rats (P < 0.01) despite a decrease in their plasma insulin concentrations (P < 0.01), whereas HD-DZ lean rats displayed a diabetic response (P < 0.01). The adipocyte-specific insulin receptor binding was dose-dependently increased in both lean and obese DZ animals (P < 0.01). DZ had a dual effect on insulin metabolism; it decreased insulin secretion and increased insulin receptor binding. This dual effect was associated with improved glucose tolerance and a decrease in weight gain in obese rats.

Adipose Tissue↗
PubMed1988

Taurine binding to the purified insulin receptor.

Taurine (2-aminoethanesulfonic acid) was shown to bind specifically and reversibly to the purified human insulin receptor. While insulin binding to the purified insulin receptor exhibited characteristic negative cooperativity and an apparent dissociation constant (Kd) of 1.2 X 10(-9) M, taurine binding was shown to exhibit positive cooperativity and had a lower affinity for the insulin receptor. The apparent Kd for taurine binding to the purified insulin receptor was calculated to be 130 X 10(-9) M and the maximum number of binding sites (Bmax) was 1.6 nmol/mg receptor protein. Chromatographic data demonstrated that taurine binds to the 138,000 molecular weight subunit of the insulin receptor. Taurine binding to the receptor protein was displaced by either taurine or insulin. Anti-human insulin receptor sera prevented insulin or taurine from binding to the receptor. Taurine binding to the protein was pH dependent, and sulfur-containing taurine analogues were able to displace taurine from the insulin receptor. These data supported our previous in vivo and in vitro observations that the hypoglycemic properties of taurine appear to be mediated through an interaction of taurine with the insulin receptor.

Humans↗
PubMed1984

Hypoglycemic properties of taurine: not mediated by enhanced insulin release.

Taurine (2-aminoethanesulfonic acid) has been shown to be a potent hypoglycemic agent in the Wistar Kyoto rat (WKY). Glucose and insulin levels were measured in serum at various times after glucose loading (400 mg/kg, i.p.). Pretreatment with taurine (200 mg/kg, i.p.) attenuated the rise in serum glucose levels at 0.5 hr after glucose administration. In addition, taurine also prevented the rise in serum immunoreactive insulin levels. The taurine analogue hypotaurine produced a similar inhibition in the rise of both serum glucose and insulin levels while beta-alanine, the carboxylic acid derivative of taurine, was totally ineffective. The enhanced glucose clearance can be explained by an increase in deoxyglucose accumulation in skeletal muscle and liver. In the liver, a 50% increase in glycogen synthesis was observed. A possible interrelationship between taurine and insulin receptor is discussed.

Animals↗
PubMedDate not supplied

Endogenous isopropanol: forensic and biochemical implications.

Concomitant findings of isopropanol and acetone in biospecimens of decedents known not to have been exposed to the alcohol prompted a study to explain its origins. Mixtures of acetone, ADH, and NADH at pHs 7.3 and 8.8 were incubated at 37 degrees C for varying intervals. Reaction products were then analyzed by headspace GC and assured identification made by GC/MS. It was found that isopropanol is produced by reduction of acetone at pH 7.3 (to a lesser extent at pH 8.8), providing evidence for an alternate metabolic route for acetone. A mechanism for this reduction is proposed. Ranges for isopropanol (in mg/dL or mg/100 g) found in unexposed decedents were: blood 1-29; liver 7-59; brain 2-12; kidney 6-26. Thus, the forensic investigator must interpret isopropanol results cautiously, particularly when low concentrations are found.

1-Propanol↗