Faculty

Fiona Gibbons, M.D.

Specialty: Pulmonary Medicine

Massachusetts General Hospital

55 Fruit Street
GRB-645
Boston, MA 02114

Publications

The following is a list of recent publications for which this Partners Asthma Center physician has been cited as an author in PubMed databases. Study abstracts have been provided for your convenience.

Schroeter, C.H., F.K. Gibbons, P.W. Finn. Development of the Early Immune System: Impact on Allergic Diseases. Immunology and Allergy Clinics of North America 22 (4): 713-736, 2002 Nov.

Gibbons, F.K., R.S. Sweeney, O.J. Manrique, P.W. Finn, et al. Two sides of the Same Story: Skin Hypersensitivity and Allergen-Specific Lymphocyte Proliferation in Patients with Asthma. AJRCCM 165(8): A560, 2002.

Galassetti, P., F. K. Gibbons, et al. (1998). "Enhanced muscle glucose uptake facilitates nitrogen efflux from exercised muscle." J Appl Physiol 84(6): 1952-9.

The hypothesis that glucose ingestion in the postexercise state enhances the synthesis of glutamine and alanine in the skeletal muscle was tested. Glucose was infused intraduodenally for 150 min (44.5 micromol . kg-1 . min-1) beginning 30 min after a 150-min period of exercise (n = 7) or an equivalent duration sedentary period (n = 10) in 18-h-fasted dogs. Prior exercise caused a twofold greater increase in limb glucose uptake during the intraduodenal glucose infusion compared with uptake in sedentary dogs. Arterial glutamine levels fell gradually with the glucose load in both groups. Net hindlimb glutamine efflux increased in response to intraduodenal glucose in exercised but not sedentary dogs (P < 0. 05-0.01). Arterial alanine levels, depleted by 50% with exercise, rose with intraduodenal glucose in exercised but not sedentary dogs (P < 0.05-0.01). Net hindlimb alanine efflux also rose in exercised dogs in response to intraduodenal glucose (P < 0.05-0.01), whereas it was not different from baseline in sedentary controls for the first 90 min of glucose infusion. Beyond this point, it, too, rose significantly. We conclude that oral glucose may facilitate recovery of muscle from prolonged exercise by enhancing the removal of nitrogen in the form of glutamine and alanine.

Galassetti, P., K. S. Hamilton, et al. (1999). "Effect of fast duration on disposition of an intraduodenal glucose load in the conscious dog." Am J Physiol 276(3 Pt 1): E543-52.

The effects of prior fast duration (18 h, n = 8; 42 h, n = 8) on the glycemic and tissue-specific responses to an intraduodenal glucose load were studied in chronically catheterized conscious dogs. [3-3H]glucose was infused throughout the study. After basal measurements, glucose spiked with [U-14C]glucose was infused for 150 min intraduodenally. Arterial insulin and glucagon were similar in the two groups. Arterial glucose (mg/dl) rose approximately 70% more during glucose infusion after 42 h than after an 18-h fast. The net hepatic glucose balance (mg. kg-1. min-1) was similar in the two groups (basal: 1.8 +/- 0.2 and 2.0 +/- 0.3; glucose infusion: -2.2 +/- 0.5 and -2.2 +/- 0.7). The intrahepatic fate of glucose was 79% glycogen, 13% oxidized, and 8% lactate release after a 42-h fast; it was 23% glycogen, 21% oxidized, and 56% lactate release after an 18-h fast. Net hindlimb glucose uptake was similar between groups. The appearance of intraduodenal glucose during glucose infusion (mg/kg) was 900 +/- 50 and 1,120 +/- 40 after 18- and 42-h fasts (P < 0.01). Conclusion: glucose administration after prolonged fasting induces higher circulating glucose than a shorter fast (increased appearance of intraduodenal glucose); liver and hindlimb glucose uptakes and the hormonal response, however, are unchanged; finally, an intrahepatic redistribution of carbons favors glycogen deposition.

Galassetti, P., M.G. Krishna, K.S. Hamilton, F.K. Gibbons, D.B. Lacy, A.D. Cherrington, and D.H. Wasserman. Effect of prior exercise on hindlimb glutamine and alanine release during intestinal glucose. The Faseb Journal 11: A142, 1997.

Hamilton, K. S., F. K. Gibbons, et al. (1996). "Effect of prior exercise on the partitioning of an intestinal glucose load between splanchnic bed and skeletal muscle." J Clin Invest 98(1): 125-35.

Exercise leads to marked increases in muscle insulin sensitivity and glucose effectiveness. Oral glucose tolerance immediately after exercise is generally not improved. The hypothesis tested by these experiments is that after exercise the increased muscle glucose uptake during an intestinal glucose load is counterbalanced by an increase in the efficiency with which glucose enters the circulation and that this occurs due to an increase in intestinal glucose absorption or decrease in hepatic glucose disposal. For this purpose, sampling (artery and portal, hepatic, and femoral veins) and infusion (vena cava, duodenum) catheters and Doppler flow probes (portal vein, hepatic artery, external iliac artery) were implanted 17 d before study. Overnightfasted dogs were studied after 150 min of moderate treadmill exercise or an equal duration rest period. Glucose ([14C]glucose labeled) was infused in the duodenum at 8 mg/kg x min for 150 min beginning 30 min after exercise or rest periods. Values, depending on the specific variable, are the mean +/- SE for six to eight dogs. Measurements are from the last 60 min of the intraduodenal glucose infusion. In response to intraduodenal glucose, arterial plasma glucose rose more in exercised (103 +/- 4 to 154 +/- 6 mg/dl) compared with rested (104 +/- 2 to 139 +/- 3 mg/dl) dogs. The greater increase in glucose occurred even though net limb glucose uptake was elevated after exercise (35 +/- 5 vs. 20 +/- 2 mg/min) as net splanchnic glucose output (5.1 +/- 0.8 vs. 2.1 +/- 0.6 mg/kg x min) and systemic appearance of intraduodenal glucose (8.1 +/- 0.6 vs. 6.3 +/- 0.7 mg/kg x min) were also increased due to a higher net gut glucose output (6.1 +/- 0.7 vs. 3.6 +/- 0.9 mg/kg x min). Adaptations at the muscle led to increased net glycogen deposition after exercise [1.4 +/- 0.3 vs. 0.5 +/- 0.1 mg/(gram of tissue x 150 min)], while no such increase in glycogen storage was seen in liver [3.9 +/- 1.0 vs. 4.1 +/- 1.1 mg/(gram of tissue x 150 min) in exercised and sedentary animals, respectively]. These experiments show that the increase in the ability of previously working muscle to store glycogen is not solely a result of changes at the muscle itself, but is also a result of changes in the splanchnic bed that increase the efficiency with which oral glucose is made available in the systemic circulation.

Wasserman, D.H., R.M. O’Doherty, F.K. Gibbons, K.S. Hamilton, A.D. Cherrington, D.K. Granner, and B.A. Zinker. Regulation of glucose fluxes during and after moderate-intensity exercise. Glucose Fluxes, Exercise, and Diabetes. Nishimura Co. Ltd., Tokyo, Japan, Chapter 2, p. 11-22, 1996.

Wasserman, D.H., F.K. Gibbons, K.A. Stokes, and B.A. Zinker. Regulation of glucose fluxes during and after muscular work. IDF Official Satellite Symposium on Glucose Fluxes, Exercise, and Diabetes ‘94, Ishiyaku Publishing Co., Tokyo, Japan, Section 3, Chapter 1: 71-85, 1996.

Stokes, K.A., F.K. Gibbons, R.D. Wilson, D.P. Bracy, and D.H. Wasserman. Mechanism of hepatic and muscle glycogen resynthesis from ingested glucose following exercise. Diabetes 43 (suppl. 1): 221 A, 1994.