. 2022 Jun;606(7915):785-790.

doi: 10.1038/s41586-022-04828-5. Epub 2022 Jun 15.

An exercise-inducible metabolite that suppresses feeding and obesity

Veronica L Li^#^{1

2

3

4}, Yang He^#⁵, Kévin Contrepois^{6

7

8}, Hailan Liu⁵, Joon T Kim^{1

3}, Amanda L Wiggenhorn^{1

2

3}, Julia T Tanzo^{1

3}, Alan Sheng-Hwa Tung^{1

3}, Xuchao Lyu^{1

3

4}, Peter-James H Zushin⁹, Robert S Jansen^{10

11}, Basil Michael⁶, Kang Yong Loh^{2

3}, Andrew C Yang¹², Christian S Carl¹³, Christian T Voldstedlund¹³, Wei Wei^{1

3

14}, Stephanie M Terrell^{1

3}, Benjamin C Moeller^{15

16}, Rick M Arthur¹⁶, Gareth A Wallis¹⁷, Koen van de Wetering^{10

18}, Andreas Stahl⁹, Bente Kiens¹³, Erik A Richter¹³, Steven M Banik^{2

3}, Michael P Snyder^{6

7

8

4}, Yong Xu^{19

20}, Jonathan Z Long^{21

22

23

24

25}

Affiliations

¹ Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
² Department of Chemistry, Stanford University, Stanford, CA, USA.
³ Sarafan ChEM-H, Stanford University, Stanford, CA, USA.
⁴ Wu Tsai Human Performance Alliance, Stanford University, Stanford, CA, USA.
⁵ Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX, USA.
⁶ Department of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
⁷ Stanford Cardiovascular Institute, Stanford University, Stanford, CA, USA.
⁸ Stanford Diabetes Research Center, Stanford University, Stanford, CA, USA.
⁹ Department of Nutrition and Toxicology, University of California Berkeley, Berkeley, CA, USA.
¹⁰ Netherlands Cancer Institute, Amsterdam, Netherlands.
¹¹ Department of Microbiology, Radboud University, Nijmegen, Netherlands.
¹² Department of Anatomy and the Bakar Aging Research Institute, University of California San Francisco, San Francisco, CA, USA.
¹³ August Krogh Section of Molecular Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark.
¹⁴ Department of Biology, Stanford University, Stanford, CA, USA.
¹⁵ Maddy Equine Analytical Chemistry Laboratory, California Animal Health and Food Safety Laboratory, School of Veterinary Medicine, University of California at Davis, Davis, CA, USA.
¹⁶ Department of Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, CA, USA.
¹⁷ School of Sport, Exercise, and Rehabilitation Sciences, College of Life and Environmental Sciences, University of Birmingham, Birmingham, UK.
¹⁸ Department of Dermatology and Cutaneous Biology, Thomas Jefferson University, Philadelphia, PA, USA.
¹⁹ Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX, USA. yongx@bcm.edu.
²⁰ Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA. yongx@bcm.edu.
²¹ Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA. jzlong@stanford.edu.
²² Sarafan ChEM-H, Stanford University, Stanford, CA, USA. jzlong@stanford.edu.
²³ Stanford Cardiovascular Institute, Stanford University, Stanford, CA, USA. jzlong@stanford.edu.
²⁴ Stanford Diabetes Research Center, Stanford University, Stanford, CA, USA. jzlong@stanford.edu.
²⁵ Wu Tsai Human Performance Alliance, Stanford University, Stanford, CA, USA. jzlong@stanford.edu.

^# Contributed equally.

PMID: 35705806
PMCID: PMC9767481
DOI: 10.1038/s41586-022-04828-5

An exercise-inducible metabolite that suppresses feeding and obesity

Veronica L Li et al. Nature. 2022 Jun.

. 2022 Jun;606(7915):785-790.

doi: 10.1038/s41586-022-04828-5. Epub 2022 Jun 15.

Authors

Affiliations

¹ Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA.
² Department of Chemistry, Stanford University, Stanford, CA, USA.
³ Sarafan ChEM-H, Stanford University, Stanford, CA, USA.
⁴ Wu Tsai Human Performance Alliance, Stanford University, Stanford, CA, USA.
⁵ Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX, USA.
⁶ Department of Genetics, Stanford University School of Medicine, Stanford, CA, USA.
⁷ Stanford Cardiovascular Institute, Stanford University, Stanford, CA, USA.
⁸ Stanford Diabetes Research Center, Stanford University, Stanford, CA, USA.
⁹ Department of Nutrition and Toxicology, University of California Berkeley, Berkeley, CA, USA.
¹⁰ Netherlands Cancer Institute, Amsterdam, Netherlands.
¹¹ Department of Microbiology, Radboud University, Nijmegen, Netherlands.
¹² Department of Anatomy and the Bakar Aging Research Institute, University of California San Francisco, San Francisco, CA, USA.
¹³ August Krogh Section of Molecular Physiology, Department of Nutrition, Exercise and Sports, Faculty of Science, University of Copenhagen, Copenhagen, Denmark.
¹⁴ Department of Biology, Stanford University, Stanford, CA, USA.
¹⁵ Maddy Equine Analytical Chemistry Laboratory, California Animal Health and Food Safety Laboratory, School of Veterinary Medicine, University of California at Davis, Davis, CA, USA.
¹⁶ Department of Molecular Biosciences, School of Veterinary Medicine, University of California, Davis, CA, USA.
¹⁷ School of Sport, Exercise, and Rehabilitation Sciences, College of Life and Environmental Sciences, University of Birmingham, Birmingham, UK.
¹⁸ Department of Dermatology and Cutaneous Biology, Thomas Jefferson University, Philadelphia, PA, USA.
¹⁹ Children's Nutrition Research Center, Department of Pediatrics, Baylor College of Medicine, Houston, TX, USA. yongx@bcm.edu.
²⁰ Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX, USA. yongx@bcm.edu.
²¹ Department of Pathology, Stanford University School of Medicine, Stanford, CA, USA. jzlong@stanford.edu.
²² Sarafan ChEM-H, Stanford University, Stanford, CA, USA. jzlong@stanford.edu.
²³ Stanford Cardiovascular Institute, Stanford University, Stanford, CA, USA. jzlong@stanford.edu.
²⁴ Stanford Diabetes Research Center, Stanford University, Stanford, CA, USA. jzlong@stanford.edu.
²⁵ Wu Tsai Human Performance Alliance, Stanford University, Stanford, CA, USA. jzlong@stanford.edu.

^# Contributed equally.

PMID: 35705806
PMCID: PMC9767481
DOI: 10.1038/s41586-022-04828-5

Abstract

Exercise confers protection against obesity, type 2 diabetes and other cardiometabolic diseases^1-5. However, the molecular and cellular mechanisms that mediate the metabolic benefits of physical activity remain unclear⁶. Here we show that exercise stimulates the production of N-lactoyl-phenylalanine (Lac-Phe), a blood-borne signalling metabolite that suppresses feeding and obesity. The biosynthesis of Lac-Phe from lactate and phenylalanine occurs in CNDP2⁺ cells, including macrophages, monocytes and other immune and epithelial cells localized to diverse organs. In diet-induced obese mice, pharmacological-mediated increases in Lac-Phe reduces food intake without affecting movement or energy expenditure. Chronic administration of Lac-Phe decreases adiposity and body weight and improves glucose homeostasis. Conversely, genetic ablation of Lac-Phe biosynthesis in mice increases food intake and obesity following exercise training. Last, large activity-inducible increases in circulating Lac-Phe are also observed in humans and racehorses, establishing this metabolite as a molecular effector associated with physical activity across multiple activity modalities and mammalian species. These data define a conserved exercise-inducible metabolite that controls food intake and influences systemic energy balance.

PubMed Disclaimer

Conflict of interest statement

Competing interest declaration

The authors declare the following competing interests: a provisional patent application has been filed by Stanford University on lactoyl amino acids for the treatment of metabolic disease.

Figures

**Extended Data Fig. 1.. Additional metabolomic characterization of Lac-Phe and lactoyl amino acid dynamics in mouse and thoroughbred racehorse exercise.**
(a) Schematic of speed and incline in the acute running protocol for mice. (b) Extracted ion chromatograms the endogenous m/z = 236.0928 peak in mouse plasma in comparison with a synthetic Lac-Phe standard. (**c,d**) Fragmentation spectra (c) extracted ion chromatogram (d) of the the endogenous m/z = 236.0928 peak in horse plasma in comparison with a synthetic Lac-Phe standard. (e) Quantitation of Lac-Phe levels in the indicated tissue from either sedentary mice (blue) or after a single bout of exhaustive running (red). (**f,g**) Quantitation of the indicated lactoyl amino acid level in blood plasma from mouse (f) or racehorse (g). For (e) and (f), N = 5/group; for (g), N=10/group. Data are shown as mean ± SEM. All experiments were performed once. P-values were calculated by Student’s two-sided t-test.

**Extended Data Fig. 2.. Additional characterization and validation of CNDP2 protein in cells and in mice.**
(a) Schematic of the chemical reaction catalyzed by CNDP2 to produce Lac-Phe. (b) *Cndp2* mRNA expression across tissues from *Tabula Muris*. (**c-e**) Anti-CNDP2 (top) and anti-tubulin (bottom) Western blots in WT and CNDP2-KO RAW264.7 (c), RT4 (d), or TKPTS (e) cells. (**f-h**) Anti-CNDP2 (top) and anti-actin (bottom) Western blots of liver (f), kidney (g), or quadraceps (h) harvested from either sedentary mice (left three lanes) or mice after a single bout of exhaustive exercise (right three lanes). For gel source data, see Supplementary Figure 1. For (c), experiments were performed twice. For (**d-h**), experiments were performed once.

**Extended Data Fig. 3.. Additional characterization of the effects of Lac-Phe administration to diet-induced obese mice.**
(**a,b**) Phenotype associations of the single nucleotide polymorphisms rs373836366 (a) and rs780772968 (b) from the Type 2 Diabetes Knowledge Portal. (**c,d**) Plasma Lac-Phe levels (c) and blood lactate levels (d) in plasma of mice following a single injection of Lac-Phe (50 mg/kg, IP). (**e-g**) 12 hr oxygen consumption VO₂ (e), carbon dioxide production VCO₂ (f), and respiratory exchange ratio RER (g) of 22-week old DIO mice following a single injection of vehicle or Lac-Phe (50 mg/kg, IP). (**h-j**) Food intake (h), kaolin intake (i), and water intake (j) in 21-week old DIO mice following a single injection of vehicle or Lac-Phe (50 mg/kg, IP). (**k,l**) Plasma leptin (k) and acyl-ghrelin (l) levels in 17-week old DIO mice 30 min after a single injection of vehicle or Lac-Phe (50 mg/kg, IP). For (c), (d), (k), and (l), N=3/group. For (**e-j**), N=7/group. Data are shown as means ± SEM. All experiments were performed once. P-values were calculated by Student’s two-sided t-test.

**Extended Data Fig. 4.. Metabolic effects of Lac-Phe administration to chow-fed, lean mice.**
(a) Lac-Phe levels in plasma of male lean mice (22–27 g) following a single injection of Lac-Phe (50 mg/kg, IP). (**b-f**) 12 h food consumption (b), ambulatory activity (c), oxygen consumption VO₂ (d), carbon dioxide production VCO₂ (e), and respiratory exchange ratio RER (f) of chow fed lean mice following a single injection of Lac-Phe (50 mg/kg, IP). (g) 24 h food intake in lean mice after a single injection of Lac-Phe at the indicated dose. For (a), N=3/group. For (**b-f**), N=8/group. For (g), N=5/group. Data are shown as means ± SEM. For (**a-f**), experiments were performed once. For (g), experiments were performed two times. P-values were calculated by Student’s two-sided t-test.

**Extended Data Fig. 5.. Metabolic effects of oral Lac-Phe administration to diet-induced obese mice.**
(**a,b**) Change in body weight (a) and daily food intake (b) of 16-week diet-induced obese mice treated with Lac-Phe (50 mg/kg/day, PO). N=5/group. Data are shown as means ± SEM. Experiments were performed once.

**Extended Data Fig. 6.. Additional characterization of CNDP2-KO mice.**
(a) Treadmill time until exhaustion for WT and CNDP2-KO (“KO”) mice. (**b-d**) Plasma levels of the indicated lactoyl amino acid in WT or CNDP2-KO mice in the sedentary state or after a single bout of acute exhaustive running (“exercise”). (e) Plasma levels of carnosine in sedentary WT or CNDP2-KO mice. (**f,g**) Body weight (f) and cumulative daily food intake (g) of WT (blue) or CNDP2-KO (red) mice under high fat diet, sedentary conditions. For (a), N=6 for WT and N=8 for CNDP2-KO; for (**b-d**), N=6/group; for (e), N=6 for WT and N=5 for CNDP2-KO; for (**f,g**), N=8 for WT and N=11 for CNDP2-KO. Data are shown as means ± SEM. For (**a-g**), experiments were performed once. P-values for (**a-e**) were calculated by Student’s two-sided t-test.

**Extended Data Fig. 7.. Plasma Lac-Phe levels in WT and ABCC5-KO mice sedentary mice or after a single bout of treadmill running to exhaustion.**
N=3/group. Data are shown as means ± SEM. Experiments were performed once. P-values were calculated by Student’s two-sided t-test.

**Extended Data Fig. 8.. Additional characterization of plasma Lac-Phe levels in humans.**
(**a,b**) Tandem MS fragmentation (a) and co-elution (b) of an authentic Lac-Phe standard and the endogenous *m/z* = 236.0928 mass from human plasma run on the Snyder laboratory untargeted metabolomics platform (see Methods). (c) Time course of phenylalanine levels in blood before and after a single acute bout of treadmill running from the human acute treadmill exercise study (Cohort 1, N=36). (d) Time course of lactate levels before and after sprint (red), resistance (blue), and endurance (light blue) exercise from the human crossover acute exercise study (Cohort 2, N=8). For (**c,d**), data are shown as mean ± SEM, **p < 0.01, ***p < 0.001. Experiments were performed once. P-values were calculated by two-way ANOVA with repeated measures.

**Fig. 1.. Lac-Phe is robustly induced in blood plasma after a single bout of running in mice and racehorses.**
(**a-d**) T-statistic of all blood plasma peaks detected by targeted (blue circles) or untargeted (grey circles) metabolomics in post-run versus control mice (a) and racehorses (c), and extracted ion chromatogram of the top *m/z* = 236.0928 mass in mice (b) and racehorses (d). (e) Tandem MS fragmentation (left) and structural assignment (right) of an authentic Lac-Phe standard (top) and endogenous *m/z* = 236.0928 mass (bottom) from mouse plasma. (**f,g**) Absolute quantitation of Lac-Phe in mouse (f) or racehorse (g) plasma. (h) Time course of Lac-Phe in blood plasma after a single bout of exhaustion running in mice. For (a), (b), and (f), N=5/group. For (c), (d), and (g), N=10/group. Data are shown as means ± SEM. The experiments in (**a-e**) were performed once; the experiments in (**f-g**) were performed three times; and the experiments in (h) were performed two times. P-values were calculated by Student’s two-sided t-test.

**Fig. 2.. CNDP2- and lactate-dependent production and secretion of Lac-Phe in vitro.**
(a) Mean *Cndp2* mRNA expression across mouse cells and tissues from Tabula Muris. Highlighted black dots, monocytes/macrophages; highlighted blue dots, epithelial cells. (**b-g**) Lac-Phe levels in conditioned media and cell lysate of WT and CNDP2-KO RAW264.7 macrophage cells (**b,c**), RT4 bladder epithelial cells (**d,e**), or TKPTS kidney epithelial cells (**f,g**) under the indicated condition. Lactate-treated cells were supplemented with 25 mM lactate for 24 h. For (**b-i**) N=3/group. Data are shown as means ± SEM. The experiments shown in (b) was performed three times and the experiments in (**c-g**) were performed once. P-values were calculated by Student’s two-sided t-test.

**Fig. 3.. Lac-Phe suppresses food intake and obesity and improves glucose homeostasis.**
(**a,b**) Cumulative food intake (a) and ambulatory activity (b) of 22-week male DIO mice following injection of either vehicle (blue) or Lac-Phe (red, 50 mg/kg, intraperitoneal [IP]). (**c,d**) Cumulative food intake (c) and change in body weight (d) of 22-week male DIO mice treated daily with vehicle (blue) or Lac-Phe (red, 50 mg/kg/day, IP). (e) Glucose tolerance test (1 g/kg glucose) of vehicle- or Lac-Phe treated mice. This assay was performed after a 6 h fast one day following the last Lac-Phe dose on day 10. (**f-g**) Tissue weights (f) and representative images of adipose tissues (g) from mice after 10 days of vehicle or Lac-Phe treatment. iWAT, inguinal white adipose tissue; eWAT, epididymal white adipose tissue; BAT, brown adipose tissue. (h) Average daily food intake (left) and change in body weight (right) of 15-week male DIO mice after 5-day treatment with vehicle (grey), Lac-Phe (red, 50 mg/kg/day, IP) or vehicle-treated pair-fed mice (blue). (i) Average daily food intake (left) and change in body weight (right) of 13-week male DIO mice after 7-day treatment with vehicle (grey), lactate (blue, 50 mg/kg/day, IP), phenylalanine (green, 50 mg/kg/day, IP), or Lac-Phe (red, 50 mg/kg/day, IP). For (**a,b**), N=6/group; for (**c-g**), N=9 for vehicle and N=8 for Lac-Phe groups; for (h), N=8 for vehicle, N=10 for Lac-Phe, and N=10 for pair fed groups; for (i), N=5/group. Data are shown as mean ± SEM. The experiments shown in (**a,b**) were performed once; the experiments shown in (**c-d**) were performed three times; and the experiments shown in (**e-i**) were performed once. P-values were calculated by two-way ANOVA with repeated measures (for **a-e**) and Student’s two-sided t-test (for **f-i**).

**Fig. 4.. Increased food intake and obesity in mice genetically deficient in Lac-Phe.**
(a) Plasma Lac-Phe levels in male WT (blue) and CNDP2 KO (red) mice under sedentary conditions or after a single bout of exhaustive treadmill running. (**b,c**) Cumulative daily food intake (b) and body weight (c) of male WT (blue) and CNDP2-KO (red) mice under an obesigenic diet/exercise training regimen in which mice were fed high fat diet (60% kcal from fat) and exercised by treadmill running 5 days/week (see Methods). (d) Change in body weight of WT (blue) and CNDP2-KO (“KO”, red) mice after 40 days of obesogenic diet alone (“HFD/Sedentary”) or obesogenic diet with treadmill running (“HFD/Exercise”). (**e,f**) Tissue weights (e) and representative images of adipose tissues (f) of WT (blue) and CNDP2-KO (red) mice following a combined obesogenic diet/treadmill running protocol. Tissue weights and images were taken on day 41. iWAT, inguinal white adipose tissue; eWAT, epididymal white adipose tissue; BAT, brown adipose tissue. For (a), N=6/group. For (**b,c**) and (**e,f**), N=8 for WT and N=8 for CNDP2-KO. For (d), N=8 for WT HFD/Sedentary, N=11 for CNDP2-KO HFD/Sedentary, N=9 for WT HFD/Exercise, and N=8 for CNDP2-KO HFD/Exercise. Data are shown as mean ± SEM. The experiments shown in (**a-c**) were performed two times and the experiments shown in (**d-f**) were performed once. P-values were calculated by two-way ANOVA with repeated measures (for **b,c**) or Student’s two-sided t-test (for a, d, and e).

**Fig. 5.. Robust and sustained elevation of Lac-Phe following human exercise.**
(a) Schematic of human acute treadmill exercise study design, N=36, “Cohort 1”. (b) Exercise-regulated metabolites (dark blue), lipids (grey), or proteins (light blue) from blood plasma in Cohort 1. A previously unassigned metabolite with a chemical formula matching that of Lac-Phe (red) was ranked the third most exercise-regulated molecule in the entire dataset. (c) Time course of Lac-Phe and lactate in blood in Cohort 1 after exercise in the non-exercised control group. (d) Schematic of human crossover acute exercise study design, N=8, “Cohort 2”. (e) Time course of Lac-Phe levels pre and post-exercise in Cohort 2. (f) Correlation of plasma Lac-Phe and lactate levels immediately pre- and post-exercise across the three exercise modalities in Cohort 2. Data are shown as mean ± SEM. The experiments were performed once. P-values were calculated by two-way ANOVA with repeated measures.

See this image and copyright information in PMC

Comment in

Exercise molecule burns away hunger.
Kim T, Sternson SM. Kim T, et al. Nature. 2022 Jun;606(7915):655-656. doi: 10.1038/d41586-022-01321-x. Nature. 2022. PMID: 35705863 No abstract available.
Mimicking the beneficial effects of exercise.
Crunkhorn S. Crunkhorn S. Nat Rev Drug Discov. 2022 Aug;21(8):555. doi: 10.1038/d41573-022-00110-5. Nat Rev Drug Discov. 2022. PMID: 35764829 No abstract available.
An exercise-induced metabolite alters feeding.
Greenhill C. Greenhill C. Nat Rev Endocrinol. 2022 Sep;18(9):521. doi: 10.1038/s41574-022-00719-x. Nat Rev Endocrinol. 2022. PMID: 35790834 No abstract available.

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An exercise-inducible metabolite that suppresses feeding and obesity

Affiliations

An exercise-inducible metabolite that suppresses feeding and obesity

Authors

Affiliations

Abstract

Conflict of interest statement

Figures

Comment in

References

Methods References

MeSH terms

Substances

Grants and funding

LinkOut - more resources

Full Text Sources

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Medical

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