This work was presented in part at the annual meeting of the American Federation for Clinical Research, Atlantic City, N. J., May 1972. Dr. Salans is the recipient of a Research Career Development Award from the Institute of Arthritis, Metabolic and Digestive Diseases of the National Institutes of Health. Dr. Cushman is a recipient of an American Diabetes Association Research and Development Award. Received for publication 5 October 1973 and in revised form 7 November 1973. changing rates of glucose oxidation and increasing rates of glucose carbon incorporation into glyceride-glycerol in the absence of insulin, but (b) decreasing stimulation of glucose oxidation by insulin. On the other hand, when cell size is kept constant, increasing dietary carbohydrate intake is associated with an increased basal rate of glucose metabolism and response to insulin by both small and large adipose cells. Thus, the rate of glucose oxidation and the magnitude of the insulin response of large adipose cells from individuals ingesting a high carbohydrate diet may be similar to or greater than that in smaller cells from individuals ingesting an isocaloric lower carbohydrate diet. The alterations in basal glucose metabolism and insulin response observed in adipose tissue from patients with spontaneous obesity are reproduced by weight gain induced experimentally in nonobese volunteers; these metabolic changes are reversible witlh weight loss. The relationships among adipose cell size, dietary composition, and the metabolism of adipose tissue are similar in spontaneous and in experimental obesity.

Woodchuck plasma was collected during four seasons of the year and assayed for total and dialyzable (free) T4 and T3 and for rT3. Plasma concentrations of total and free T4 and T3 were higher in the spring (T4, 5.4 +/- 0.6 microgram/dl; free T4, 3.0 +/- 0.4 ng/dl; T3, 202 +/- 22 ng/dl; free T3, 0.51 +/- 0.04 ng/dl) and lower in the prehibernatory fattening period in summer (T4, 2.3 +/- 1.0 microgram/dl; free T4, 1.2 +/- 0.5 ng/dl; T3, 45 +/- 27 ng/dl; free T3, 0.16 +/- 0.10 ng/dl) and fall (T4, 3.2 +/- 1.0 microgram/dl; free T4, 1.3 +/- 0.2 ng/dl; T3, 130 +/- 12 ng/dl; free T3, 0.25 +/- 0.02 ng/dl). In spite of the extremely high concentrations of T3 in the winter (437 +/- 32 ng/dl), free T3 concentrations (0.034 +/- 0.003 ng/dl), when measured at the appropriate temperature for hibernation, were significantly lower than those found at other seasons of the year. Plasma binding of T3 was lower during the summer and increased again to approximately double the spring value during the winter. rT3 was at or below the sensitivity of the method (6 ng/dl) at all seasons. It is suggested that the wide seasonal variations in thyroid hormone concentrations and altered plasma protein binding may represent important adaptations influencing the metabolic rate and the process of hibernation in the woodchuck.

Metabolic, respiratory and haematological parameters were investigated for the Little Pocket mouse during circadian torpor cycles. The rate of O2, consumption decreased from 7.04 to 0.05 ml O2· g−1· hr−1, with a corresponding decrease in respiratory minute volume from 49.4 to 0.9 ml · min−1 during torpor at an ambient temperature of 10 C.No changes in haemoglobin concentration (19.7 g/100 ml), haematocrit (54 %), red blood corpuscle count (12.4 106/μl), mean corpuscular volume (43.6 μm3), mean corpuscular haemoglobin content (16.2 pg), mean corpuscular haemoglobin concentration (37.4 %) and [2,3-DPG] (9.6 μmol/g Hb) were observed during torpor cycles.The half saturation tension of P. longimembris haemoglobin was 41 mm Hg (37 C, pH = 7.28) and 19.7 mmHg (10 C, pH = 7.51).The effect of temperature on P50was Δlog P50/ C = + 0.0106(pH = 7.4).Venous blood parameters were: euthermic mice (37 C); PCO2 = 36.8 mm Hg, PO2 = 49.5 mm Hg, pH = 7.28,[HCO3−] = 17.3mmol/l ; torpid mice (10 C) ; PCO2 = 14.6,PO2 = 35.7,pH = 7.51,[HCC3] = 18.8. These data indicate a new, relatively acidotic acid-base status during torpor, characterised by a higher H+/OH− ratio.The respiratory sensitivity to inspired CO2 of pocket mice was, despite their being semi-fossorial, typical of other mammals. High concentrations of CO2, did not induce, or facilitate, entry into torpor.