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While maintained under all combinations of three temperatures and two RH, fifth instar larvae of the Mediterranean flour moth, Ephestia kuehniella were fed wheat treated with spores and crystals of Bacillus thuringiensis var. kurstaki. Larvae that had fed on wheat with the bacterial preparation contained higher concentrations of nodules in their haemocoel than did larvae fed on wheat without bacteria. Nodule concentrations in larvae fed untreated wheat were unaffected by temperature or relative humidity. Larvae fed treated wheat had higher nodule concentrations at 32 degrees C than at 15 and 23 degrees C, and higher nodule concentrations at a relative humidity of 85% than at 43%. The percentage of larvae that pupated was lower when larvae were fed the bacterial preparation, and was significantly higher at 23 degrees C than at 15 and 32 degrees C, regardless of whether larvae were fed bacteria or not. Less time was required for larvae to develop to pupation at higher temperatures and at higher humidity. Mean time to pupation was lower for bacteria-fed larvae than for those fed untreated wheat, and this appeared to be a result of truncation of the distribution of times to pupation because only rapidly developing larvae survived to pupation.

Canadian and French laboratory strains of Sitophilus granarius (L.) and Cryptolestes ferrugineus (Stephens) were cold acclimated by placing adults at 15, 10 and 5 degrees C successively for 2wk at each temperature before deacclimating them for 1wk at 30 degrees C. Unacclimated S. granarius had an LT(50) (lethal time for 50% of the population) of 12days at 0 degrees C compared with 40days after the full cold acclimation. At -10 degrees C, unacclimated C. ferrugineus had an LT(50) of 1.4days compared with 24days after the full acclimation. Cold acclimation was lost within a week after returning insects to 30 degrees C. Trehalose, as well as the amino acids proline, asparagine, glutamic acid and lysine were higher in cold acclimated insects for both species. For S. granarius, glutamine was higher in cold acclimated insects and isoleucine, ethanolamine and phosphoethanolamine, a precursor of phospholipids, were lower in cold acclimated insects. For C. ferrugineus, alanine, aspartic acid, threonine, valine, isoleucine, leucine, phenylalanine and phosphoethanolamine were higher in cold acclimated insects. For both species tyrosine was lower in cold acclimated insects. There were small but significant differences between Canadian and French strains of S. granarius, with the Canadian strain being more cold hardy and having higher levels of trehalose. There were small but significant differences between male and female S. granarius, with males being more cold hardy and having higher levels of proline, asparagine and glutamic acid. In conclusion, high levels of trehalose and proline were correlated with cold tolerance, as seen in several other insects. However, correlation does not prove that these compounds are responsible for cold tolerance, and we outline further tests that could demonstrate a causal relationship between trehalose and proline and cold tolerance.

Gastric inhibitory polypeptide (GIP) has insulinotropic actions in the presence of hyperglycemia. However, its extrapancreatic effects on glucose homeostasis are controversial. We have studied the relationships between GIP and immunoreactive insulin (IRI) and glucose turnover rates (D3H-3 glucose technique) in five poorly controlled type II diabetic patients and five normal subjects before and after a breakfast containing 500 kcal including 42 g sucrose. Mean fasting serum glucose levels and glucose responses were significantly (P less than 0.001) higher in the diabetic patients than in normal subjects. Mean basal serum IRI levels were similar in both groups [12.8 +/- 2.9 (SEM) vs. 11.8 +/- 2 microU/ml, P = NS]. After meal ingestion, mean IRI levels rose significantly to a peak at 20 min in the normal subjects but the responses were blunted in the diabetic patients (74 +/- 10 vs. 24 +/- 6 microU/ml, P less than 0.001). At all other times studied (60-180 min), mean serum IRI levels were similar in the diabetic patients and the normal subjects except at 180 min. Mean basal serum GIP levels were similar in the diabetic patients and the normal subjects (538 +/- 100 vs. 400 +/- 50 pg/ml, P = NS). After meal ingestion, mean GIP levels rose between 0-60 min but were significantly higher in the diabetic patients only at 20 min (1200 +/- 190 vs. 566 +/- 76 pg/ml, P less than 0.01). Mean basal hepatic glucose output was higher (P less than 0.01) in the diabetic patients. However, the mean basal MCR values were similar. After meal ingestion, total splanchnic glucose output and rates of glucose utilization (RU) were significantly higher in the diabetic patients compared with the normal subjects (P less than 0.001, and P less than 0.001, respectively). Postmeal MCR values were not statistically different in both groups. There were significant positive correlations between postmeal splanchnic glucose output and both IRI (r = 0.805, P less than 0.005) and GIP (r = 0.749, P less than 0.02) in the diabetic patients but not in the normal subjects (r = 0.10, P = NS for both). Whereas no relationships existed between RU and IRI in either group, RU correlated strongly with GIP (r = 0.810, P less than 0.005) only in the diabetic patients. We hypothesize that GIP may play a compensatory role to improve both impaired beta-cell insulin release and peripheral glucose utilization which are the recognized pathogenetic mechanisms underlying type II diabetes mellitus.

The brachial artery pressure and retinal artery pressure responses to a one-minute cold pressor test were evaluated simultaneously in 14 patients with type I diabetes mellitus (six with and eight without diabetic retinopathy) and 10 age-matched control subjects. Five patients with type I diabetes had autonomic neuropathy. Mean baseline brachial artery pressure and retinal artery pressure were similar in patients with type I diabetes and control subjects. After cold pressor testing, the brachial artery pressure increased significantly (p less than 0.01) compared with baseline values in both groups. Retinal mean arterial pressures increased significantly (p less than 0.001) after cold pressor testing compared with the baseline values only in patients with type I diabetes. Positive correlation was found between the brachial and retinal mean arterial pressures after cold pressor testing (r = 0.48; p less than 0.05) in the diabetic patients but not in the control subjects (r = 0.10; p = NS). No correlation was found between the retinal artery pressure and age of onset of diabetes, duration of diabetes, the presence or absence of diabetic retinopathy, and glycemic control. Four patients with autonomic neuropathy and low retinal artery pressures, which remained unchanged after cold pressor testing, had no diabetic retinopathy. The fifth patient with autonomic neuropathy and exaggerated systolic brachial artery pressure (175 mm Hg) and retinal artery pressure (more than 80 mm Hg) responses had severe background diabetic retinopathy. In conclusion, abnormal retinal artery responses to stress are present in patients with type I diabetes. This may be modified by the presence or absence of both autonomic neuropathy and hypertension. The biologic significance of these findings is yet to be determined.