Biomedical subjects

T S David

Publications and source records attributed to T S David.

6 recordsLinked to original sources

PubMed1998

Sphingomyelinase has an insulin-like effect on glucose transporter translocation in adipocytes.

Rat epididymal adipocytes were incubated with 0, 0.1, and 1 mU sphingomyelinase/ml for 30 or 60 min, and glucose uptake and GLUT-1 and GLUT-4 translocation were assessed. Adipocytes exposed to 1 mU sphingomyelinase/ml exhibited a 173% increase in glucose uptake. Sphingomyelinase had no effect on the abundance of GLUT-1 in the plasma membrane of adipocytes. In contrast, 1 mU sphingomyelinase/ml increased plasma membrane content of GLUT-4 by 120% and produced a simultaneous decrease in GLUT-4 abundance in the low-density microsomal fraction. Sphingomyelinase had no effect on tyrosine phosphorylation of either the insulin receptor beta-subunit or the insulin receptor substrate-1, a signaling molecule in the insulin signaling pathway. It is concluded that the incubation of adipocytes with sphingomyelinase results in insulin-like translocation of GLUT-4 to the plasma membrane and that this translocation does not occur via the activation of the initial components of the insulin signaling pathway.

Adipocytes↗

PubMed1997

Phosphatidylinositol 3-kinase and dynamics of insulin resistance in denervated slow and fast muscles in vivo.

Regulation of glucose uptake by 1- and 3-day denervated soleus (slow-twitch) and plantaris (fast-twitch) muscles in vivo was investigated. One day after denervation, soleus and plantaris muscles exhibited 62 and 65% decreases in insulin-stimulated 2-deoxyglucose uptake, respectively, compared with corresponding control muscles. At this interval, denervated muscles showed no alterations in insulin receptor binding and activity, amount and activity of phosphatidylinositol 3-kinase, and amounts of GLUT-1 and GLUT-4. Three days after denervation, there was no increase in 2-deoxyglucose uptake in response to insulin in soleus muscle, whereas plantaris muscle exhibited a 158% increase in basal and an almost normal absolute increment in insulin-stimulated uptake. Despite these differences, denervated soleus and plantaris muscles exhibited comparable decreases in insulin-stimulated activities of the insulin receptor (approximately 40%) and phosphatidylinositol 3-kinase (approximately 50%) and a pronounced decrease in GLUT-4. An increase in GLUT-1 in plantaris, but not soleus, muscle 3 days after denervation is consistent with augmented basal 2-deoxyglucose uptake in plantaris muscle at this interval. These results demonstrate that, in denervated muscles, there is a clear dissociation between insulin-stimulated 2-deoxyglucose uptake and upstream events involved in insulin-stimulated glucose uptake.

Animals↗

PubMed1997

Growth hormone-induced insulin resistance: role of the insulin receptor, IRS-1, GLUT-1, and GLUT-4.

Treatment of rats with growth hormone (GH; 1 mg/kg sc) twice daily over 2.5 days did not alter fasting plasma glucose or glucose tolerance but increased fasting plasma insulin levels 65% and peak insulin response to a glucose load 35% over controls, indicating the development of insulin resistance. Studies on partially purified insulin receptors from soleus muscles showed that GH increased the abundance of insulin receptor beta-subunits by 48% as measured by immunoblotting. Despite this increase, GH abolished the increase in autophosphorylation of the insulin receptor beta-subunit in response to physiological hyperinsulinemia and diminished by 28% the response to supraphysiological hyperinsulinemia. Similarly, insulin-stimulated phosphorylation of insulin receptor substrate-1 (IRS-1) was decreased 25% by GH, but the abundance of IRS-1 was not affected. Studies on rats pretreated with streptozotocin suggested that the effects of GH are direct and not secondary to GH-induced hyperinsulinemia. GH decreased basal GLUT-1 abundance in the low-density microsome and plasma membrane fractions of epididymal adipocytes by 50 and 42%, respectively, but decreased basal GLUT-4 abundance only in the low-density microsome fraction by 24%. Despite these alterations, the abundance of both transporters in the plasma membrane fraction of adipocytes incubated with 0.1 U insulin/ml was not diminished by GH.

Adipocytes↗

PubMed1995

Insulin-stimulated phosphatidylinositol 3-kinase activity and 2-deoxy-D-glucose uptake in rat skeletal muscles.

To date there is suggestive evidence that phosphatidylinositol 3-kinase participates in insulin-stimulated glucose transport. However, its involvement in skeletal muscle, a major site of insulin-stimulated glucose disposal, has not been addressed. Therefore, we tested the effects of wortmannin, a known inhibitor of phosphatidylinositol 3-kinase, on insulin-stimulated 2-deoxyglucose uptake by rat soleus muscle in vitro: Wortmannin (1 microM) reversibly inhibited insulin-induced 2-deoxyglucose uptake in soleus muscle by 44%. Inclusion of 5 microM wortmannin in the incubation medium completely abolished the insulin-induced increment in 2-deoxyglucose uptake. In conclusion, the insulin-signaling cascade linking insulin-receptor tyrosine kinase activation to glucose uptake in skeletal muscle.

Androstadienes↗

PubMedDate not supplied

Electrothermally-assisted capsular shift.

The marriage of biomedical instrumentation and patient care has once again proven itself successful. The ETAC is a new procedure with various potential applications. Despite its embryonic stage, this procedure is being used by a handful of shoulder surgeons who are cautiously pursuing new and improved ways to prevent the common and debilitating diagnosis of shoulder instability. Follow-up thus far is short, and the current literature lacks studies that compare the time-honored conventional standard of open stabilization to this new procedure. However, those surgeons who have been using this device are optimistic about its role in the future repair of shoulder injuries.

Arthroscopy↗

PubMedDate not supplied

Perioperative lower urinary tract infections and deep sepsis in patients undergoing total joint arthroplasty.

Deep sepsis in the involved joint after hip or knee arthroplasty may be the result of hematogenous seeding from a remote infectious source. This mechanism has been used to explain the well-documented association between postoperative urinary tract infections and subsequent joint infection after hip or knee arthroplasty. However, it is unclear whether there is an association between preoperative bacteriuria and deep prosthetic infection. The purpose of this review is to identify perioperative risk factors associated with bacteriuria that have a positive correlation with deep joint sepsis following total hip or knee arthroplasty. The classic symptoms of dysuria, urgency, and frequency seen with urinary tract infections are often absent in the elderly despite the presence of urine coliforms; in these patients, pyuria (as indicated by the presence of more than 1x10(3) white blood cells per milliliter of noncentrifuged urine) may be used as a preliminary screening criterion. If there are irritative symptoms, the presence of more than 1x10(3) bacteria per milliliter of urine should be regarded as indicative of a urinary tract infection. If there is bacteriuria without symptoms of urinary irritation or obstruction, the current literature supports proceeding with total joint arthroplasty and treating those patients with urine colony counts greater than 1x10(3)/mL with an 8- to 10-day postoperative course of an appropriate oral antibiotic. Postponement of total joint surgery should be considered if preoperative evaluation reveals symptoms related to obstruction of the urinary pathway. Irritative symptoms in combination with a bacterial count greater than 1x10(3)/mL should also serve as an indication to postpone surgery. To diminish postoperative urinary tract infection, a bladder catheter should be inserted immediately preoperatively and removed within 24 hours of surgery to diminish the risk of urinary retention, which has been shown to increase the likelihood of a postoperative urinary tract infection.

Algorithms↗