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J Turinsky

Publications and source records attributed to J Turinsky.

8 recordsLinked to original sources
PubMed1992

Effect of sphingoid bases on basal and insulin-stimulated 2-deoxyglucose transport in skeletal muscle.

Incubation of rat soleus muscles with 50 microM sphingosine or 50 microM sphinganine augmented basal 2-deoxy-D-glucose (2DG) transport 32%, but reduced the response to 0.1 and 1.0 mU insulin/ml by 17 and 27%, respectively. When the muscles were incubated with 50 microM phytosphingosine, a 63-93% increase in basal 2DG transport was observed. However, this treatment had no effect on insulin-stimulated 2DG transport. The phytosphingosine-induced increase in basal 2-DG transport was inhibited 93 and 98% with 35 and 70 microM cytochalasin B, respectively, suggesting that it is mediated by glucose transporters. Cellular accumulation of L-glucose, which is not mediated by glucose transporters, was not affected by phytosphingosine. It is concluded that (a) both sphingosine and sphinganine increase basal 2DG transport in muscle but diminish insulin-stimulated transport, and (b) phytosphingosine stimulates basal 2DG transport in muscle by a mechanism involving glucose transporters.

Animals↗
PubMed1992

Modulation of prostaglandin E2 synthesis in rat skeletal muscle.

The effect of muscle denervation, inhibitors of protein synthesis, G proteins, and sphingolipids on prostaglandin E2 (PGE2) release by rat soleus muscle in vitro was investigated. To assess the effect of muscle denervation, the sciatic nerve in one hindlimb of rats was interrupted, and soleus muscles from the denervated hindlimb and the contralateral sham (control) hindlimb were excised 1-5 days after surgery. Compared with corresponding sham muscles, PGE2 release by denervated muscles was increased 56, 230, and 435% at 1, 3, and 5 days after denervation, respectively. Protein synthesis inhibitors cycloheximide (10 microM) and puromycin (10 microM) lowered PGE2 release by sham and denervated muscles 62-80%. The release of PGE2 by sham and denervated muscles was not altered by pertussis toxin (1 microgram/ml) but was inhibited 30-51% by AlF4-. Addition of 100 microM guanosine 5'-O-(3-thiotriphosphate) to saponin-permeabilized sham and denervated muscles had only a moderate, if any, stimulatory effect on PGE2 release. This effect was not counteracted by 1 mM guanosine 5'-O-(2-thiodiphosphate). Increasing muscle ceramide concentration by incubation with sphingomyelinase (100 mU/ml) increased PGE2 release by sham and denervated muscles 43 and 157%, respectively. Because degradation of ceramides yields sphingosine, the effect of sphingosine was also tested. Sphingosine (25 microM) increased PGE2 release by sham and denervated muscles 139 and 187%, respectively, without affecting muscle viability, as assessed by the release of lactate dehydrogenase. The data indicate that muscle denervation, treatment with sphingomyelinase, and sphingosine stimulate, whereas inhibitors of protein synthesis inhibit PGE2 synthesis by muscle.

Aluminum↗
PubMed1979

Macrophage dysfunction after burn injury.

The phagocytic and microbicidal activities of alveolar and peritoneal macrophages were evaluated 4 and 24 h after a full-thickness scald burn of 26 to 28% body surface area in anesthetized rats. The contribution of serum factors to the macrophage functions was studied concurrently. The phagocytic activity of alveolar macrophages obtained 4 or 24 postburn was reduced approximately 65% below control values when they were incubated in media containing autologous serum and approximately 45% (below controls) when they were incubated in media containing normal (control) serum. A similar, although not as marked, decrease in the phagocytic activity of peritoneal macrophages was also demonstrated. Serum obtained from rats 4 or 24 h postburn had a significant suppressive effect on the phagocytic activity of control alveolar, but not peritoneal, macrophages. The intracellular microbicidal activity of peritoneal macrophages obtained at the postburn intervals and incubated in media containing either autologous or control serum was unaltered from control values. However, alveolar macrophages obtained 24 h, but not 4 h, postburn had a significant (approximately 80%) increase, above control values, in their microbicidal activity. Serum obtained 24 h, but not 4 h, postburn stimulated control alveolar macrophage killing ability. These data indicate that thermal injury induces a defect in the phagocytic activity rather than the microbicidal activity of macrophages. This phagocytic alteration is mediated, in part, by serum.

Animals↗
PubMed1979

Biphasic alterations in glucose metabolism by soleus muscle from the burned limb.

Tissue temperature and in vitro glucose metabolism by rat soleus muscle were studied following a 3-second burn on one hind limb in 90 degrees C water. The injury increased the subcutaneous temperature in the calf of the burned limb to 53.4 +/- 0.7 (SE) degrees C and that between soleus muscle and fibula to 49.4 +/- 1.3 degrees C, both temperatures returning to normal at approximately 3 minutes postburn. The injury resulted in biphasic alterations in glucose metabolism by the soleus muscle from the burned limb; glucose uptake and lactate release were depressed at 4 hours but were elevated above control levels at 3 days postburn. The maintenance of an approximate 1:2 ratio of glucose uptake to lactate release suggested that changes in glucose uptake reflected primarily conversion to tricarbon units rather than changes in the rate of glucose oxidation. Since glucose metabolism by soleus muscle from contralateral unburned limb of injured animals did not differ from controls at any of the test times, the changes in the burned limb were not likely the result of systemic alterations in metabolic and endocrine environment. The biphasic alterations did not correlate with the degree of soleus muscle edema. It is concluded that proximity to the burn wound is a new determinant of abnormal glucose utilization by skeletal muscle.

Animals↗
PubMed1978

The insulin concentration in human ocular fluids.

We measured immunoreactive insulin concentrations in ocular fluids and serum of 19 patients. In rhegmatogenous retinal detachment patients without diabetes mellitus, the serum insulin level was 7 +/- 2 (SE) microunits/ml and the subretinal fluid insulin levels were mostly undetectable. By contrast, in rhegmatogenous retinal detachment patients with diabetes mellitus, serum insulin was 35 +/- 5 microunits/ml and the subretinal fluid always contained low but detectable amojnts of insulin. The data may suggest a small leak of insulin into the subretinal fluid of rhegmatogenous retinal detachment patients with diabetic retinopathy. In vitrectomy patients with diabetes mellitus there was no insulin in the vitreous in eight out of nine cases.

Body Fluids↗
PubMed1977

Dynamics of insulin secretion and resistance after burns.

Alteration in the insulin regulation of carbohydrate metabolism following 20% surface burn injury in the rat was biphasic. At 4 hr after burn there was fasting hyperglycemia (92 +/- 6 (SE) mg/100 ml above controls) and a pronounced intolerance to 1 gm glucose/kg IV. Fasting serum insulin did not differ from controls and failed to rise appreciably following glucose administration. Two to four days after burn, the ability to cope with exogenous glucose was near normal or normal and the insulin response to standard glucose load was 41-69% higher than in the controls, indicating the presence of insulin resistance. This pattern was not altered by feeding the burned and control rats with glucose intragastrically, thus eliminating lower postburn food intake as the causal factor of exaggerated insulin response to IV glucose. Diaphragms from burned rats showed the same increase in glucose uptake in response to 0.1 U insulin/ml in vitro as those of controls, suggesting that the insulin resistance in vivo is not due to a decrease in the capacity of muscle to bind and respond to insulin.

Animals↗
PubMedDate not supplied

Local effect of burn injury on glucose and amino acid metabolism by skeletal muscle.

Previous studies from our laboratory demonstrated that there is a difference in glucose metabolism by skeletal muscles from the burned versus unburned regions of the body. To further investigate the effect of proximity to the burn wound on muscle metabolism, in vitro glucose uptake as well as lactic and amino acid releases by soleus muscles, were studied 3 days following a 3-second scald burn on one hind limb of the rat. No differences in glucose uptake or lactic and amino acid releases were observed between soleus from the unburned limb of burned rats and that of controls. In comparison to these two groups, soleus from the burned limb took up 125% more glucose (p less than 0.001), and released 80% more lactic acid (p less than 0.01), 229% more alanine (p less than 0.001), 84% more glutamic acid (p less than 0.01), and over 36% more glutamine (p less than 0.05). The relatively enhanced release of lactic acid by soleus muscle from the burned limb was reduced but not eliminated by the omission of glucose from the medium. Simultaneously, the omission of glucose had no effect on the release of alanine, glutamic acid, and glutamine by the burned limb soleus. The data indicate that a mild thermal injury stimulates glucose utilization and enhances amino acid release by skeletal muscle from the burned region. Since such an effect is absent in muscle from the contralateral unburned region of the same animal, the changes are not likely to be mediated by systemic alterations in the metabolic and endocrine environment. The persistence of an enhanced amino acid release in the presence of varying glycolytic rates suggests that the burn-induced local alterations in amino acid metabolism by skeleton muscle are independent of coincident changes in glucose utilization.

Amino Acids↗