Changes In Energy Availability Research Articles

Regulation of Microalgal Photosynthetic Electron Transfer.

The global ecosystem relies on the metabolism of photosynthetic organisms, featuring the ability to harness light as an energy source. The most successful type of photosynthesis utilizes a virtually inexhaustible electron pool from water, but the driver of this oxidation, sunlight, varies on time and intensity scales of several orders of magnitude. Such rapid and steep changes in energy availability are potentially devastating for biological systems. To enable a safe and efficient light-harnessing process, photosynthetic organisms tune their light capturing, the redox connections between core complexes and auxiliary electron mediators, ion passages across the membrane, and functional coupling of energy transducing organelles. Here, microalgal species are the most diverse group, featuring both unique environmental adjustment strategies and ubiquitous protective mechanisms. In this review, we explore a selection of regulatory processes of the microalgal photosynthetic apparatus supporting smooth electron flow in variable environments.

KATP channels are necessary for glucose-dependent increases in amyloid-β and Alzheimer's disease-related pathology.

Elevated blood glucose levels, or hyperglycemia, can increase brain excitability and amyloid-β (Aβ) release, offering a mechanistic link between type 2 diabetes and Alzheimer's disease (AD). Since the cellular mechanisms governing this relationship are poorly understood, we explored whether ATP-sensitive potassium (KATP) channels, which couple changes in energy availability with cellular excitability, play a role in AD pathogenesis. First, we demonstrate that KATP channel subunits Kir6.2/KCNJ11 and SUR1/ABCC8 were expressed on excitatory and inhibitory neurons in the human brain, and cortical expression of KCNJ11 and ABCC8 changed with AD pathology in humans and mice. Next, we explored whether eliminating neuronal KATP channel activity uncoupled the relationship between metabolism, excitability, and Aβ pathology in a potentially novel mouse model of cerebral amyloidosis and neuronal KATP channel ablation (i.e., amyloid precursor protein [APP]/PS1 Kir6.2-/- mouse). Using both acute and chronic paradigms, we demonstrate that Kir6.2-KATP channels are metabolic sensors that regulate hyperglycemia-dependent increases in interstitial fluid levels of Aβ, amyloidogenic processing of APP, and amyloid plaque formation, which may be dependent on lactate release. These studies identify a potentially new role for Kir6.2-KATP channels in AD and suggest that pharmacological manipulation of Kir6.2-KATP channels holds therapeutic promise in reducing Aβ pathology in patients with diabetes or prediabetes.

The dynamics of the diversity–energy relationship during the last 21,000 years

AbstractAimSpatial diversity patterns are linked to energy availability, but how the diversity–energy relationship changes in space and time is unclear. There are three possible scenarios: (a) equilibrium dynamics, where diversity is always positively related to energy availability in both time and space; (b) out‐of‐equilibrium dynamics, where diversity is determined by energy availability in equilibrium, but diversity variation lags behind changes in energy availability, leading to a mismatch between temporal and spatial diversity–energy relationships; and (c) disequilibrium dynamics where the equilibrium does not exist or is irrelevant. We attempt to distinguish these scenarios using spatio‐temporal palaeoecological data.LocationUSA and Canada.Time period21,000–1,000 years before present.Major taxa studiedWoody plants.MethodsWe tested for the strength and direction of temporal and spatial relationships between pollen type diversity of woody species and energy availability (estimated from temperature and precipitation) in 1,000‐year time steps.ResultsWhereas the temporal diversity–energy relationship appears only when energy levels rapidly change, the spatial diversity–energy relationship is pronounced only when these levels stabilize.Main conclusionsOur findings are consistent with the out‐of‐equilibrium scenario – diversity equilibria do exist and act as attractors of diversity dynamics, but diversity is often out of equilibrium. Consequently, current rapid climate changes can disrupt spatially consistent diversity–energy relationships. To understand diversity dynamics, it is crucial to simultaneously consider both the spatial and temporal dimensions of diversity variation.

The Molecular Brakes of Adipose Tissue Lipolysis.

Adaptation to changes in energy availability is pivotal for the survival of animals. Adipose tissue, the body’s largest reservoir of energy and a major source of metabolic fuel, exerts a buffering function for fluctuations in nutrient availability. This functional plasticity ranges from energy storage in the form of triglycerides during periods of excess energy intake to energy mobilization via lipolysis in the form of free fatty acids for other organs during states of energy demands. The subtle balance between energy storage and mobilization is important for whole-body energy homeostasis; its disruption has been implicated as contributing to the development of insulin resistance, type 2 diabetes and cancer cachexia. As a result, adipocyte lipolysis is tightly regulated by complex regulatory mechanisms involving lipases and hormonal and biochemical signals that have opposing effects. In thermogenic brown and brite adipocytes, lipolysis stimulation is the canonical way for the activation of non-shivering thermogenesis. Lipolysis proceeds in an orderly and delicately regulated manner, with stimulation through cell-surface receptors via neurotransmitters, hormones, and autocrine/paracrine factors that activate various intracellular signal transduction pathways and increase kinase activity. The subsequent phosphorylation of perilipins, lipases, and cofactors initiates the translocation of key lipases from the cytoplasm to lipid droplets and enables protein-protein interactions to assemble the lipolytic machinery on the scaffolding perilipins at the surface of lipid droplets. Although activation of lipolysis has been well studied, the feedback fine-tuning is less well appreciated. This review focuses on the molecular brakes of lipolysis and discusses some of the divergent fine-tuning strategies in the negative feedback regulation of lipolysis, including delicate negative feedback loops, intermediary lipid metabolites-mediated allosteric regulation and dynamic protein–protein interactions. As aberrant adipocyte lipolysis is involved in various metabolic diseases and releasing the brakes on lipolysis in thermogenic adipocytes may activate thermogenesis, targeting adipocyte lipolysis is thus of therapeutic interest.

Triiodothyronine and cortisol levels in the face of energetic challenges from reproduction, thermoregulation and food intake in female macaques

Energy availability drives an individual's fitness and can be affected by diverse energetic challenges. The assessment of hormones involved in metabolic activity and energy mobilization provides a gateway to the study of physiological adaptations in response to changes in energy availability. Here, we investigated immunoreactive urinary total triiodothyronine (uTT3, thyroid hormone secreted through the hypothalamus-pituitary-thyroid axis and regulating the basal metabolic rate) alongside glucocorticoids (i.e. urinary cortisol, uCort, secreted through the hypothalamus-pituitary-adrenal axis and mediating energy mobilization) in wild female Assamese macaques (Macaca assamensis). Combining more than 2900; of behavioral data from 42 adult females with physiological data from 382 urine samples, we evaluated both uTT3 and uCort in relation to potential energetic challenges encountered by a female, namely fluctuations in energy intake, travel distance, reproductive state and minimum ambient temperature. As predicted, levels of both hormones changed in response to variation in energy intake with a tendency toward a positive effect on uTT3 and a significant negative effect on uCort levels. Unexpectedly, neither hormone was influenced by variation in travel distance. Reproductive state affected both hormones with higher levels of uTT3 and uCort in the second half of gestation. Finally, a decrease of minimum temperature triggered an increase in uCort but unexpectedly not in uTT3. Collectively, our results highlight the respective contribution of two endocrine axes when facing energetic challenges and the underlying metabolic strategies to cope with them. Overall, assessing thyroid hormones together with glucocorticoids provides an integrative picture in the evaluation of an individual's energy status.

The ‘Jekyll and Hyde’ of Gluconeogenesis: Early Life Adversity, Later Life Stress, and Metabolic Disturbances

The physiological response to a psychological stressor broadly impacts energy metabolism. Inversely, changes in energy availability affect the physiological response to the stressor in terms of hypothalamus, pituitary adrenal axis (HPA), and sympathetic nervous system activation. Glucocorticoids, the endpoint of the HPA axis, are critical checkpoints in endocrine control of energy homeostasis and have been linked to metabolic diseases including obesity, insulin resistance, and type 2 diabetes. Glucocorticoids, through the glucocorticoid receptor, activate transcription of genes associated with glucose and lipid regulatory pathways and thereby control both physiological and pathophysiological systemic energy homeostasis. Here, we summarize the current knowledge of glucocorticoid functions in energy metabolism and systemic metabolic dysfunction, particularly focusing on glucose and lipid metabolism. There are elements in the external environment that induce lifelong changes in the HPA axis stress response and glucocorticoid levels, and the most prominent are early life adversity, or exposure to traumatic stress. We hypothesise that when the HPA axis is so disturbed after early life adversity, it will fundamentally alter hepatic gluconeogenesis, inducing hyperglycaemia, and hence crystalise the significant lifelong risk of developing either the metabolic syndrome, or type 2 diabetes. This gives a “Jekyll and Hyde” role to gluconeogenesis, providing the necessary energy in situations of acute stress, but driving towards pathophysiological consequences when the HPA axis has been altered.

Measuring PGC-1α and Its Acetylation Status in Mouse Primary Myotubes.

Metabolic flexibility is vital for organisms to respond to and survive changes in energy availability. A critical metabolic flexibility regulator is peroxisome proliferator-activated receptor γ coactivator 1α (PGC-1α), which regulates various transcription factors and nuclear receptors that, in turn, regulate mitochondrial homeostasis and fatty acid oxidation. PGC-1α is itself regulated, with one of the significant modes of regulation being acetylation. Thus, measuring the acetylation status of PGC-1α is a critical indicator of cells' metabolic flexibility. In this chapter, we describe a method of evaluating PGC-1α acetylation in primary mouse myotubes. This method can also be used with other cell types and tissues.

Elevated energy requirement of cone photoreceptors

We have used recent measurements of mammalian cone light responses and voltage-gated currents to calculate cone ATP utilization and compare it to that of rods. The largest expenditure of ATP results from ion transport, particularly from removal of Na+ entering outer segment light-dependent channels and inner segment hyperpolarization-activated cyclic nucleotide-gated channels, and from ATP-dependent pumping of Ca2+ entering voltage-gated channels at the synaptic terminal. Single cones expend nearly twice as much energy as single rods in darkness, largely because they make more synapses with second-order retinal cells and thus must extrude more Ca2+ In daylight, cone ATP utilization per cell remains high because cones never remain saturated and must continue to export Na+ and synaptic Ca2+ even in bright illumination. In mouse and human retina, rods greatly outnumber cones and consume more energy overall even in background light. In primates, however, the high density of cones in the fovea produces a pronounced peak of ATP utilization, which becomes particularly prominent in daylight and may make this part of the retina especially sensitive to changes in energy availability.

PHD3 Loss Promotes Exercise Capacity and Fat Oxidation in Skeletal Muscle

Rapid alterations in cellular metabolism allow tissues to maintain homeostasis during changes in energy availability. The central metabolic regulator acetyl-CoA carboxylase 2 (ACC2) is robustly phosphorylated during cellular energy stress by AMP-activated protein kinase (AMPK) to relieve its suppression of fat oxidation. While ACC2 can also be hydroxylated by prolyl hydroxylase 3 (PHD3), the physiological consequence thereof is poorly understood. We find that ACC2 phosphorylation and hydroxylation occur in an inverse fashion. ACC2 hydroxylation occurs in conditions of high energy and represses fatty acid oxidation. PHD3-null mice demonstrate loss of ACC2 hydroxylation in heart and skeletal muscle and display elevated fatty acid oxidation. Whole body or skeletal muscle-specific PHD3 loss enhances exercise capacity during an endurance exercise challenge. In sum, these data identify an unexpected link between AMPK and PHD3, and a role for PHD3 in acute exercise endurance capacity and skeletal muscle metabolism.

Phenotypic heterogeneity as key factor for growth and survival under oligotrophic conditions.

Productivity-poor oligotrophic environments are plentiful on earth. Yet it is not well understood how organisms maintain population sizes under these extreme conditions. Most scenarios consider the adaptation of a single microorganism (isogenic) at the cellular level, which increases their fitness in such an environment. However, in oligotrophic environments, the adaptation of microorganisms at population level - that is, the ability of living cells to differentiate into subtypes with specialized attributes leading to the coexistence of different phenotypes in isogenic populations - remains a little-explored area of microbiology research. In this study, we performed experiments to demonstrate that an isogenic population differentiated to two subpopulations under low energy-flux in chemostats. Fluorescence cytometry and turnover rates revealed that these subpopulations differ in their nucleic acid content and metabolic activity. A mechanistic modelling framework for the dynamic adaptation of microorganisms with the consideration of their ability to switch between different phenotypes was experimentally calibrated and validated. Simulation of hypothetical scenarios suggests that responsive diversification upon a change in energy availability offers a competitive advantage over homogenous adaptation for maintaining viability and metabolic activity with time.

2294-PUB: Investigating Medial Amygdala Circuits in Glucose Homeostasis

One out of every 10 Americans has diabetes, increasing their risk of death by 50% and more than doubling their health care costs. Delineating how the brain regulates metabolism, including feeding behavior and glucose homeostasis, may shed light on how those processes are altered in disease. The medial amygdalar nucleus (MeA) regulates the intersection of stress, social behavior, and metabolism. Fos expression in the MeA of mice is altered by changes in energy availability - fasting/re-feeding and hyper-/hypoglycemia - suggesting this nucleus may regulate feeding behavior and blood glucose levels in response to internal cues. The primary downstream targets of the MeA are the principle nucleus of the bed nucleus of the stria terminalis (prBNST) and ventromedial hypothalamus (VMH), regions previously shown to regulate metabolism. Cfos immunohistochemistry and retrograde labeling show that MeA neurons that project to the VMH (MeA-->VMH) are preferentially activated by a 36h fast, compared to ad libitum feeding and a 1h refeed. Selectively activating MeA-->VMH neurons using chemogenetics induces hyperglycemia independent of changes to circulating insulin and changes in feeding. Ongoing fos, axonal tracing, and behavioral studies aim to delineate the contributions of different MeA cell types to glucose homeostasis in the context of other competing behaviors including social interaction and stress. Disclosure K. Devarakonda: None. K. Conner: None. D. Garibay: None. S. Stanley: None. Funding American Diabetes Association/Pathway to Stop Diabetes (1-17-ACE-31 to S.S.); American Heart Association (18PRE33960254)

Microtubule-dependent and independent roles of spastin in lipid droplet dispersion and biogenesis.

Lipid droplets (LDs) are metabolic organelles that store neutral lipids and dynamically respond to changes in energy availability by accumulating or mobilizing triacylglycerols (TAGs). How the plastic behavior of LDs is regulated is poorly understood. Hereditary spastic paraplegia is a central motor axonopathy predominantly caused by mutations in SPAST, encoding the microtubule-severing protein spastin. The spastin-M1 isoform localizes to nascent LDs in mammalian cells; however, the mechanistic significance of this targeting is not fully explained. Here, we show that tightly controlled levels of spastin-M1 are required to inhibit LD biogenesis and TAG accumulation. Spastin-M1 maintains the morphogenesis of the ER when TAG synthesis is prevented, independent from microtubule binding. Moreover, spastin plays a microtubule-dependent role in mediating the dispersion of LDs from the ER upon glucose starvation. Our results reveal a dual role of spastin to shape ER tubules and to regulate LD movement along microtubules, opening new perspectives for the pathogenesis of hereditary spastic paraplegia.

Metabolic Niches and Biodiversity: A Test Case in the Deep Sea Benthos

The great anthropogenic alterations occurring to carbon availability in the oceans necessitates an understanding of the energy requirements of species and how changes in energy availability may impact biodiversity. The deep oceans are characterized naturally by extremely low availability of chemical energy and are particularly vulnerable to changes in carbon flux from surface waters. Because the energetic requirements of an organism impact nearly every aspect of their ecology and evolution, we hypothesize that species are adapted to specific levels of carbon availability and occupy a particular metabolic niche. We test this hypothesis in deep-sea invertebrates specifically examining how energetic demand, axes of the metabolic niche, and geographic range size vary over gradients of chemical energy availability. We find that species with higher energetic expenditures, and ecologies associated with high energy demand, are located in areas with higher chemical energy availability. In addition, we find that range size and location of deep-sea species is determined by geographic patterns in chemical energy availability. Our findings indicate that deep-sea species are adapted to specific energy regimes, the metabolic niche can potentially link scales from individuals to ecosystems, and link adaptation to patterns in biogeography and biodiversity.

The impact of agricultural input subsidies on food and nutrition security: a systematic review

Agricultural input subsidies, a form of social protection, are often considered an important means of improving agricultural productivity in low- and middle-income countries. However, their effectiveness and efficiency remains contentious with respect to productivity, economic and consumer welfare measures, as well as food and nutrition security. This is exacerbated by a weak evidence base, including no review focused on the impact of agricultural input subsidies on food security and nutrition. Further, where studies have considered nutritional outcomes of agricultural input subsidy interventions, this has often been in regard to changes in consumption of the targeted staple food, measured in terms of calorie consumption or a similar measure of changes in energy availability, ignoring other aspects of malnutrition, including impacts from dietary diversity. This wider consideration of impacts from dietary diversity is important, given the increasing recognition in nutrition policy of its importance. We address this gap in the literature with a review of the evidence on the impact of agricultural input subsidy programmes on nutrition and nutrition-related health in low- and middle-income countries, mapping this evidence against a conceptual framework of the mediating pathways.

Involvement of the SnRK1 subunit KIN10 in sucrose-induced hypocotyl elongation

ABSTRACTA mechanism participating in energy sensing and signalling in plants involves the regulation of sucrose non-fermenting1 (Snf1)-related protein kinase 1 (SnRK1) activity in response to sugar availability. SnRK1 is thought to regulate the activity of both metabolic enzymes and transcription factors in response to changes in energy availability, with trehalose-6-phospate functioning as a signalling sugar that suppresses SnRK1 activity under sugar-replete conditions. Sucrose supplementation increases the elongation of hypocotyls of developing Arabidopsis seedlings, and this response to sucrose involves both the SnRK1 subunit KIN10 and also TREHALOSE-6-PHOSPHATE SYNTHASE1 (TPS1). Here, we measured sucrose-induced hypocotyl elongation in two insertional mutants of KIN10 (akin10 and akin10-2). Under short photoperiods, sucrose supplementation caused great proportional hypocotyl elongation in these KIN10 mutants compared with the wild type, and these mutants had shorter hypocotyls than the wild type in the absence of sucrose supplementation. One interpretation is that SnRK1 activity might suppress hypocotyl elongation in the presence of sucrose, because KIN10 overexpression inhibits sucrose-induced hypocotyl elongation and akin10 mutants enhance sucrose-induced hypocotyl elongation.

MTORC1 in AGRP neurons integrates exteroceptive and interoceptive food-related cues in the modulation of adaptive energy expenditure in mice.

Energy dissipation through interscapular brown adipose tissue (iBAT) thermogenesis is an important contributor to adaptive energy expenditure. However, it remains unresolved how acute and chronic changes in energy availability are detected by the brain to adjust iBAT activity and maintain energy homeostasis. Here, we provide evidence that AGRP inhibitory tone to iBAT represents an energy-sparing circuit that integrates environmental food cues and internal signals of energy availability. We establish a role for the nutrient-sensing mTORC1 signaling pathway within AGRP neurons in the detection of environmental food cues and internal signals of energy availability, and in the bi-directional control of iBAT thermogenesis during nutrient deficiency and excess. Collectively, our findings provide insights into how mTORC1 signaling within AGRP neurons surveys energy availability to engage iBAT thermogenesis, and identify AGRP neurons as a neuronal substrate for the coordination of energy intake and adaptive expenditure under varying physiological and environmental contexts.

Bioenergetic calculations evaluate changes to habitat quality for salmonid fishes in streams treated with salmon carcass analog

Nutrient supplementation in oligotrophic streams is proposed as a means of mitigating losses of marine-derived subsidies from declining or extirpated populations of anadromous fishes. One of the central predictions of nutrient addition is an increased production of fish through bottom-up increases in invertebrate abundance. Such changes in food availability may increase growth and production rates for stream fishes by increasing habitat quality. In this study we apply bioenergetic calculations to estimate changes to habitat quality based on predicted increases in net energy intake. We compared invertebrate drift abundance and estimated changes in energy availability in streams treated with salmon carcass analog versus untreated controls. Our results revealed a two- to threefold increase in invertebrate drift abundance following the addition of salmon carcass analog; however, this effect appeared to be short-term. Measures of the energetic profitability of stream habitat for salmonid fishes revealed small, yet significant, increases in net energy availability in streams that received analog additions, but only after controlling for differences in physical habitat features such as temperature and stream flow.

Ecophysiology of cognition: How do environmentally induced changes in physiology affect cognitive performance?

Cognitive performance is based on brain functions, which have energetic demands and are modulated by physiological parameters such as metabolic hormones. As both environmental demands and environmental energy availability change seasonally, we propose that cognitive performance in free-living animals might also change seasonally due to phenotypic plasticity. This is part of an emerging research field, the 'ecophysiology of cognition': environmentally induced changes in physiological traits, such as blood glucose and hormone levels, are predicted to influence cognitive performance in free-living animals. Energy availability for the brain might change, and as such cognition, with changing energetic demands (e.g. reproduction) and changes of energy availability in the environment (e.g. winter, drought). Individuals spending more energy than they can currently obtain from their environment (allostatic overload type I) are expected to trade off energy investment between cognition and other life-sustaining processes or even reproduction. Environmental changes reducing energy availability might thus impair cognition. However, selection pressures such as predation risk, mate choice or social demands may act on the trade-off between energy saving and cognition. We assume that different environmental conditions can lead to three different trade-off outcomes: cognitive impairment, resilience or enhancement. Currently we cannot understand these trade-offs, because we lack information about changes in cognitive performance due to seasonal changes in energy availability and both the resulting changes in homeostasis (for example, blood glucose levels) and the associated changes in the mechanisms of allostasis (for example, hormone levels). Additionally, so far we know little about the fitness consequences of individual variation in cognitive performance. General cognitive abilities, such as attention and associative learning, might be more important in determining fitness than complex and specialized cognitive abilities, and easier to use for comparative study in a large number of species. We propose to study seasonal changes in cognitive performance depending on energy availability in populations facing different predation risks, and the resulting fitness consequences.

Decreased Energy Availability during Intensified Training Increases Fatigue and Reduces Performance in Competitive Female Runners

PURPOSE: Functional overreaching (F-OR) is a state of high perceived fatigue and decreased performance, resulting from high training loads combined with inadequate recovery. While F-OR athletes show some performance gains after a taper period, the magnitude of these gains may be reduced compared to athletes who avoid F-OR during intensified training. As no studies have quantified the influence of changes in energy availability (EA) during intense training on F-OR and performance adaptations, we tested the hypothesis that athletes’ ability to maintain EA during high training loads would influence the occurrence of F-OR and subsequent training adaptations. METHODS: 12 eumenorrheic female distance runners followed a 10-week protocol with 3 phases: P1; 4 weeks of normal training volume, P2; 4 weeks at 130% of P1 volume, and P3; 2 weeks of taper at 50% of P1 volume. Over the last 7 days of each phase, runners wore a validated activity monitor 24hrs/day to assess active energy expenditure (AEE), comprised of training-specific exercise (ExEE) and habitual activity (HaEE) and logged all energy intake (EI). At the end of each phase, runners completed the REST-Q and a hunger questionnaire, and body composition was measured by DEXA. After 36 hours of rest, they performed a graded running test to volitional exhaustion. RESULTS: ExEE increased by 36% from P1 to P2 (450 to 550 kcal/d), and perceived fatigue increased significantly (+55±17%). While hunger ratings increased significantly (63 ± 15%), mean EI only increased by 86 ± 70 kcal/d (4%, NS); only 6 of the 12 runners increased EI. Mean EA did not decrease significantly (-1.3± 3.8%), however Δ EA was correlated to Δ EI but not to Δ ExEE or Δ HaEE. Importantly, [INCREMENT]EA from P1 to P2 was also directly correlated to Δ running performance, ΔVO2peak, Δ lean body mass (R= 0.80, 0.70 and 0.92), and inversely correlated to Δlack of energy from the REST-Q and Δ perceived exertion during submaximal exercise (R= -0.85,-0.72). Furthermore, the 6 runners displaying F-OR and decreased EA at P2 showed reduced performance gains at P3 (p=0.05) compared to the runners who did not develop F-OR. CONCLUSIONS: Our results emphasize the importance of maintaining EA during critical periods of intensified training, in order to avoid F-OR and to optimize the magnitude of performance gains after a taper period.

Water yield responses to climate change and variability across the North–South Transect of Eastern China (NSTEC)

summary China is facing a growing water crisis due to climate and land use change, and rise in human water demand across this rapidly developing country. Understanding the spatial and temporal ecohydrologic responses to climate change is critical to sustainable water resource management. We investigated water yield (WY) responses to historical (1981–2000) and projected potential climate changes across a large and complex climatic and land cover gradients over the North–South Transect of Eastern China (NSTEC, a standard terrestrial transect of the International GeoBiological Project, IGBP). After an annual scale evapotranspiration (ET) model was validated with historical streamflow records from ten watersheds, the model was applied to the NSTEC that encompasses seven climatic zones. We found that (1) The spatial and temporal variations of WY were highly dependent on precipitation (P) patterns during 1981– 2000. Overall, the influences of significant temperature (T) rise on the trend of WY were suppressed by the insignificant P change during 1981–2000. (2) The long-term mean WY by climatic zone had a similar pattern as P. The different climatic zones had differential contributions to the total volumetric WY of the NSTEC. Within each climatic zone, the volumetric WY for each land cover type was highly dependent on its area of each land cover. (3) Corresponding to the P pattern, the mean WY decreased from the low (South) to high latitude (North), but the rates of changes varied along the NSTEC. Along the NSTEC, the sensitivity of WY to potential T and P changes increased from the high latitude to the low latitude. Future potential changes in WY are likely to follow changes in P with some modification by changes in energy availability. We conclude that precipitation is a major driver for water resource availability, and reliable prediction of future precipitation change patterns is critical to hydrologic forecast across the study region.