To investigate the temporal response of the liver to insulin and portal glucose delivery, somatostatin was infused into four groups of 42-h-fasted, conscious dogs ( n ϭ 6/group), basal insulin and glucagon were replaced intraportally, and hyperglycemia was created via a peripheral glucose infusion for 90 min (period 1). This was followed by a 240-min experimental period (period 2) in which hyperglycemia was matched to period 1 and either no changes were made (CON), a fourfold rise in insulin was created (

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At specific locations within the Baltic Sea, thermoclines and haloclines can create rapid spatial and temporal changes in temperature (T) and salinity (S) exceeding 10A degrees C and 9 psu with seasonal ranges in temperature exceeding 20A degrees C. These wide ranges in abiotic factors affect the distribution and abundance of Baltic Sea copepods via species-specific, physiological-based impacts on vital rates. In this laboratory study, we characterized the influence of T and S on aspects of reproductive success and naupliar survival of a southwestern Baltic population of Temora longicornis (Copepoda: Calanoida). First, using ad libitum feeding conditions, we measured egg production (EP, no. of eggs female(-1) day(-1)) at 12 different temperatures between 2.5 and 24A degrees C, observing the highest mean EP at 16.9A degrees C (12 eggs female(-1) day(-1)). Next, the effect of S on EP and hatching success (HS, %) was quantified at 12A degrees C for cohorts that had been acclimated to either 8, 14, 20 or 26 psu and tested at each of five salinities (8, 14, 20, 26 and 32 psu). The mean EP was highest for (and maximum EP similar among) 14, 20 and 26 psu cohorts when tested at their acclimation salinity whereas EP was lower at other salinities. For adults reared at 8 psu, a commonly encountered salinity in Baltic surface waters, EP was relatively low at all test salinities-a pattern indicative of osmotic stress. When incubated at 12A degrees C and 15 different salinities between 0 and 34 psu, HS increased asymptotically with increasing S and was maximal (82.6-84.3%) between 24 and 26 psu. However, HS did depend upon the adult acclimation salinity. Finally, the 48-h survival of nauplii hatched and reared at 14 psu at one of six different temperatures (10, 12, 14, 16, 18 and 20A degrees C) was measured after exposure to a novel salinity (either 7 or 20 psu). Upon exposure to 7 psu, 48-h naupliar mortality increased with increasing temperature, ranging from 26.7% at 10A degrees C to 63.2% at 20A degrees C. In contrast, after exposure to 20 psu, mortality was relatively low at all temperatures (1.7% at 10A degrees C and a parts per thousand currency sign26.7% for all other temperatures). An intra-specific comparison of EP for three different T. longicornis populations revealed markedly different temperature optima and clearly demonstrated the negative impact of brackish (Baltic) salinities. Our results provide estimates of reproductive success and early survival of T. longicornis to the wide ranges of temperatures and salinities that will aid ongoing biophysical modeling examining climate impacts on this species within the Baltic Sea

Peck, M. A., Kanstinger, P., Holste, L., and Martin, M. 2012. Thermal windows supporting survival of the earliest life stages of Baltic herring (Clupea harengus). – ICES Journal of Marine Science, 69: 529–536. Projecting climate-driven changes in marine systems will require knowledge on how thermal windows affect the vital rates of key species. To examine the potential, direct effect of climate-driven warming on southwest Baltic herring, we quantified the survival, development, and biochemical condition of embryos (eggs and yolk-sac larvae) at ten temperatures between 2.9 and 21.7°C. Viable hatch was highest from 7 to 13°C, <20% at 2.9°C and 0% at 21.7°C. Between 5 and 19°C, increasing temperature (T) decreased the time to 50% hatch (Ht, h,): Ht = 4461.9 × T − 1.24 (r2 = 0.98, p < 0.0001). Using degree-days [°d = T (°C) × age (d)] could normalize some (but not all) thermal effects. Most hatching occurred 90–120°d post-fertilization, unfed larvae lost 0.33 µg dry mass (DM) °d−1, larvae did not survive >160°d post-hatch. RNA–DNA ratios rapidly decreased between 50 and 80°d post-hatch, whereas DNA ×DM−1 increased throughout the yolk-sac phase and likely provides a stronger indicator of irreversible starvation. The critical, “mixed feeding” stage is likely 60–100°d post-hatch. The broad thermal tolerance of herring embryos makes “direct”, negative effects of warming unlikely; however, a lack of common methods among studies makes it difficult to project how climate warming will affect embryos of different fish populations and species.

We assessed basal glucose metabolism in 16 female nonpregnant (NP) and 16 late-pregnant (P) conscious, 18-h-fasted dogs that had catheters inserted into the hepatic and portal veins and femoral artery approximately 17 days before the experiment. Pregnancy resulted in lower arterial plasma insulin (11 +/- 1 and 4 +/- 1 microU/ml in NP and P, respectively, P < 0.05), but plasma glucose (5.9 +/- 0.1 and 5.6 +/- 0.1 mg/dl in NP and P, respectively) and glucagon (39 +/- 3 and 36 +/- 2 pg/ml in NP and P, respectively) were not different. Net hepatic glucose output was greater in pregnancy (42.1 +/- 3.1 and 56.7 +/- 4.0 micromol. 100 g liver(-1).min(-1) in NP and P, respectively, P < 0.05). Total net hepatic gluconeogenic substrate uptake (lactate, alanine, glycerol, and amino acids), a close estimate of the gluconeogenic rate, was not different between the groups (20.6 +/- 2.8 and 21.2 +/- 1.8 micromol. 100 g liver(-1). min(-1) in NP and P, respectively), indicating that the increment in net hepatic glucose output resulted from an increase in the contribution of glycogenolytically derived glucose. However, total glycogenolysis was not altered in pregnancy. Ketogenesis was enhanced nearly threefold by pregnancy (6.9 +/- 1.2 and 18.2 +/- 3.4 micromol. 100 g liver(-1).min(-1) in NP and P, respectively), despite equivalent net hepatic nonesterified fatty acid uptake. Thus late pregnancy in the dog is not accompanied by changes in the absolute rates of gluconeogenesis or glycogenolysis. Rather, repartitioning of the glucose released from glycogen is responsible for the increase in hepatic glucose production.

This study examined whether physiological changes in glucagon alter net hepatic glucose uptake (NHGU) or glycogen synthesis under conditions of hyperglycemia, hyperinsulinemia, and portal vein glucose concentrations exceeding those in the arterial circulation. Somatostatin was infused into 42-h-fasted dogs, insulin and glucagon were replaced intraportally at basal rates, and peripheral infusion of glucose maintained the hepatic glucose load twofold basal for 90 min (period 1). In period 2 (240 min) the insulin infusion was increased fourfold, glucose was infused intraportally, the hepatic glucose load was twofold basal, and glucagon was infused to create levels 150% basal (HiGGN, n = 6) or 40% basal (LoGGN, n = 6). NHGU rates (mg.kg-1.min-1) were low during period 1 (-0.9 +/- 0.7 in LoGGN and -0.2 +/- 0.4 in HiGGN, not significant) but increased during period 2 (-4.1 +/- 0.6 in LoGGN and -1.9 +/- 0.2 in HiGGN, P < 0.05). Endogenous glucose production (Endo Ra) declined during period 2 in LoGGN (P < 0.01 vs. basal) but did not change in HiGGN. Tracer-determined hepatic glucose uptake did not differ between groups. The poststudy increment in liver glycogen synthase I (12.5 +/- 3 vs. 6.5 +/- 2% of total) was greater in LoGGN (P < 0.05), as was net glycogen synthesis (27 +/- 8 vs. 13 +/- 3 mg/g liver, P = 0.06). An elevation in glucagon reduced NHGU (because of failure to suppress Endo Ra) and glycogen synthase activation and tended to reduce glycogen deposition.

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