Annals of Clinical and Experimental Metabolism

Central Nervous System Regulation of Appetite in Humans and Pet Animals

Review Article | Open Access | Volume 2 | Issue 1

  • 1. Department of Health, President, Hemopet, USA
+ Show More - Show Less
Corresponding Authors
odds WJ, Department of Health, President, Hemopet, 938 Stanford Street, Santa Monica, California 90403, USA, Tel: 131-082-84804; Fax: 13104535240;

Weight gain leading to obesity in humans and their companion pet animals has become of national and international concern. This problem began centuries ago with the evolutionary, genomic and eipgenomic changes that came about when human populations shifted from hunters and gatherers to farmers. The resulting lifestyle and dietary changes also affected the domestication and diet of their animal companions, especially the dog, as well as the gut microbiota they share. Appetite is controlled in individuals by their feelings of bunger and satiety (the so-called appestat), and is regulated centrally through the hypothalamus and brain stem. The hypothalamus induces secretion of the hormones adiponectin (regulates insulin secretion and fatty acid oxidation), and leptin and ghrelin (the ‘stop’ and ‘go’ hunger hormones, respectively). Leptin comes from white adipose tissue cells and decreases appetite. The gut hormones like ghrelin, cholecystokinin, other pancreatic, neuro- and glucagonlike peptides, and oxyntomodulin are produced peripherally, and decrease appetite. Basically, these hormones act as signals for satiety, which regulates food intake. Leptin and serotonin function in separate systems to control appetite. The future success of appetite control for humans and pet animals will depend upon use of effective targeted pharmacological agents in conjunction with dietary modification and lifestyle changes.


 Appetite ; Adiponectin ; Leptin ;Ghrelin ;Satiety


Dodds WJ (2017) Central Nervous System Regulation of Appetite in Humans and Pet Animals. Ann Clin Exp Metabol 2(1): 1013


CNS: Central Nervous System; 5-HT: 5-Hydroxytryptamine; GI: Gastrointestinal; CCK: Cholecystokinin; NPYY: Neuropeptide YY; POMC: Pro-opiomelanocortin; MC-4: Melanocortin-4; CRF: Corticotrophin-releasing Factor; CART: Cocaine and Amphetamine-Regulated Transcript; PP: Pancreatic Polypeptide; GLP-1: Glucagon-Like Peptide


There is a rising worldwide epidemic of obesity in humans and companion pet animals [1-5]. The World Health Organization forecasted that about 2.3 billion adults worldwide would be overweight and more than 700 million would be obese by 2015 [5]. Given their parallel evolutionary, dietary, and lifestyle adaptations, pet obesity has likewise become an epidemic [3]. A 2012 survey conducted by the Association for Pet Obesity Prevention revealed that 52.5% of dogs and 58.3% of cats were overweight or obese [4]. The most common endocrine disorders of dogs and cats are hypothyroidism and diabetes, respectively; both of which lead to obesity [3,6]. Banfield Pet Hospital’s State of Pet Health Report 2012 provides startling insight into the link between obesity and illness. The report, which analyzed data from more than two million dogs and 430 thousand cats, found that [6]:

• 42% of dogs with diabetes are overweight (and 40% of cats).

• 40% of dogs with arthritis are overweight (and 37% of cats).

• More than 40% of dogs with high blood pressure are overweight.

• 61% of hypothyroid dogs are overweight.


Evolution, genomic and epigenomic adaptations

Evolutionary changes over centuries along with the concurrent interactions between the genomic and epigenomic environments have had major influences on the microbiota of the gut in all mammals including humans [7-10]. As mammals evolved, so did their gut microbes; the host diet and phylogeny (evolutionary history) both influencing gut bacterial diversity which then became increased as one traverses from carnivores to omnivores to herbivores [7].

Ancient human populations shifted from hunters and gatherers to farmers, such that human lifestyles and diet changes also affected the domestication and diet of the dogs that accompanied them [7,9,11]. A bio cultural co evolution occurred that affected both dog genes and human culture [9]. The genetic and epigenetic characteristics of the canine genome were transformed, so that dogs developed an increased number of Amy2B gene copies coding for pancreatic amylase. This allowed them to adapt more readily and thrive on an omnivorous diet rich in starches, in comparison to the strictly carnivorous diet of their ancestor, the wolf [9].

Intestinal microbiota

The estimated bacterial content of the mammalian Gitract is approximately 1014 bacteria [12,13]. Co-habiting family members and their dogs have been shown to share microbiota with one another [11]. Thus, direct and frequent contact with our cohabitant humans and animals could significantly shape the composition of the shared microbial environment [11]. While the shared gut microbiota logically could lead to the parallel consequences of weight gain and obesity in both species, this hypothesis is still unproven [8,13]. Additionally, indigenous microbiota within the GI tract can extract calories from the otherwise in digestible common polysaccharides found in daily diets [7]. Gut microbiota can also regulate the brain-gutaxis [8,10,12-17]. The gut microbiome can stimulate vagal sensory neurons, which is a major neural pathway that conveys information from the GI luminal contents to the brain and modulates GI motility and feeding behavior [5,13-20]. The gut microbiome can influence neuronal signaling to the brain through vagalaerent neurons [5,10,16-23]. 

Body fat regulating hormones and cytokines

As the number of fat cells in the body increases, the secretion of pro-inflammatory cytokines increases in parallel, thereby creating more chronic, systemic inflammation [24,25]. The fat regulating hormones are adiponectin and leptin [5,24-30]. Adiponectin is reduced in obesity and increased in response to fasting, whereas leptin has opposite effects [5,28]. Bio active peptides such as leptin, adiponectin, and pro-inflammatory cytokines secreted from the adipose tissue are called adipokines [23-26]. Serotonin (5-hydroxytryptamine; 5-HT) is biochemically derived from tryptophan and is mainly found in the gastrointestinal (GI) tract, platelets, and central nervous system (CNS) [26-29]. In coordination with the hypothalamus, 5-HT and the brain stem regulate appetite, eating behavior, energy balance and weight [27-31]. 5-HT also plays an important role in controlling carbohydrate (sugars, starches, and cellulose) intake [26,27].

Brain sites of appetite regulation

The hypothalamus and the brain stem are central sites of appetite regulation; the midbrain is also involved [5,14- 18,31]. The hypothalamus and brain stem control carbohydrate metabolism [27]. In the canine study of de Lartigue and colleagues [23], leptin concentrations were high erin the obese group of dog’s compared to those of the lean group. Adiponectin and cerebro spinal fluid 5-HT concentrations were high erin the lean group than in the obese group. Analysis of the microbiome revealed that the diversity of the microbial community was lower in the obese group. Microbes from the phylum Firmicutes (85%) were the pre dominant group in the gut microbiota of lean dogs.

However, bacteria from the phylum Proteobacteria (76%) were the predominant group in the gut microbiota of dogs in the obese group. Similar findings were recently published [8]. Whether dysbiosis induces the development of obesity or whether obesity causes the dysbiosis of gut microbiota in unknown [23]. Leptin is also capable of regulating the endogenous production of glucose both dependently and independently of the hypothalamus and brain stem [27].

Obesity Genes

Scientists have identified “obesity gene” variants in people, however many lean individual people and pets carry these obesity genes and never become overweight [25,32].This means that the determining factor for becoming obese may be an individual’s lifestyle [7,9,21,27].

One meta-analysis of data from more than 200,000 people who carry a specific gene predisposing them to obesity found that physically active adults who carried the obesity gene were nearly one-third less likely to become overweight or obese than those who didn’t exercise [2]. Genetic predisposition does not mean that obesity is our destiny, or our dog’s destiny [32,33]. This parallel between the spike in human obesity and obesity in companion animals has developed over the last half-century and is unsettling [3,4,32,33]. It appears to relate to the similar environmental and lifestyle changes that have occurred [2,3,9- 12,21,27].


Brain regulation of appetite

Appetite: The desire to eat, is regulated by interaction between the digestive tract, adipose tissue and the brain [5,21- 31]. During stress, appetite levels may increase, whereas dysregulation of appetite leads to anorexia nervosa, cachexia, bulimia, overeating and binge eating [20-23]. Regulation of eating in the sense of hunger or satiety is termed the appestat [18].

Hypothalamus: The hypothalamus is the main regulatory effect or organ of appetite, and controls the volume of food consumed [14-16,20-23,27,31]. It communicates with other CNS areas of the brain stem and reward-related limbic pathways of the midbrain [5,16,31]. The hypothalamus also acts as a sensor via numerous hormones, discussed below, and as a biological clock that stimulates hunger. Hunger occurs when the body’s store of nutrients is depleted: short-term reservoir stores are carbohydrates; long-term reservoir stores are fat [18,31]. The glucose that regulates short-term control over appetite, and the lipostat controls long-term appetite through its cumulative effect over time [16,18]. The hypothalamus interprets and integrates the input of neural and humoral factors that result in the body’s coordinated feeding and energy expenditure responses. Certain gut hormones including ghrelin, neuropeptide YY (NPYY), pancreatic polypeptide, glucagon-like-peptide 1 (GLP-1) and oxyntomodulin, play a physiological role in governing satiety through the hypothalamus [5,16,20,23].

Brain stem: The brain stem transfers information from the peripheral nervous system to the mid- and forebrain [5,16,20]. It directly connects with the gut by neuronal pathways and regulates mechanical processes involving appetite and food intake such as chewing and swallowing [21]. The brain stem can organize certain aspects of feeding behavior without input from the hypothalamus [20]. It is also involved in regulation of energy balance. Satiety signals from the GI tract are relayed to the area postrema of the brain’s fourth ventricle via the sensory vagus nerves [5,16,20].

Midbrain: The midbrain reward system partakes in control of hedonic feeding (intake of palatable foods) which can override satiety signals [5,20].

Peripheral regulation of appetite

The peripheral appetite regulatory mechanisms can be classified as adipostat factors and gut hormones [5,19-21,23]:

Adipostat factors: The hormone leptin was discovered in 1994; it is excreted by adipocytes in white adipose tissue. Leptin has a long half-life and circulates in plasma at concentrations proportional to an individual’s fat mass, although women have much higher leptin concentrations than men [30]. Its effects are mediated by the hypothalamus in a fat regulation feedback loop, controlled by central and peripheral circadian clocks. The central circadian (hypothalamic) clock regulates weight control and long term energy balance. The peripheral circadian clock regulates leptin transcription in adipose tissue [16,23]. Circadian disruption is associated with obesity [34].

Obese individuals often have leptin resistance; and congenital leptin deficiency in mice and children results in obesity [21]. However, leptin resistance is not the only reason for obesity, as recent studies in mice have implicated circadian clock dysfunction [34]. Even chronic jet lag is sufficient to induce central leptin resistance independent of other risk factors [34]. Fertility is also affected. Insulin is secreted in response to meals and increases body stores of glycogen, fat and protein [20]. It plays a similar role to leptin, and causes obesity and diabetes; insulin-deficient animals are hyperphagic [26]. Both leptin and insulin are anorexigenic (anti-appetite stimulating) hormones. The brain regulates glucose flow from the liver [20].

Gut hormones: Post-prandial satiety is signaled by a gut sensor system [5,20]. GI hormones working with the liver transfer information to both the hypothalamus and brain stem [20]. Cholecystokinin (CCK) is the first gut hormone known to control appetite [23,24]. Digestive products in the gut lumen release this kinin from the proximal small intestine. The effects are mediated by the vagal nerve and result in anorexia [5,20,22,23]. Dietary fiber is anti-obesity and anti-diabetic; it induces neo gluco genesis when fermented by intestinal microbiota and this regulates energy homeostasis not only by metabolism of nutrients but also by the gut-brain neural network [20]. Ghrelin is the only known peripherally active appetite-stimulating (orexigenic) hormone, and relays hunger signals [5,20,21]. It is an endogenous growth hormone secretagogue, and novel orexigenic peptide that antagonizes leptin action through activation of the hypothalamic neuropeptide NPYY receptor pathway [5,20]. The major source of ghrelin is the stomach. It is a potent stimulator of food intake and growth hormone secretion. Plasma levels are inversely correlated with body weight. Blood levels rise during fasting and fall rapidly after a meal, so ghrelin output is regulated by caloric intake [21].

Pancreatic polypeptide (PP) and neuropeptide NPYY

These are anorectic gut hormones [5,16,20,22]. PP is found mostly in the pancreas, and its release is stimulated by food intake. It modulates gastric acid secretion and gastrointestinal motility; but inhibits pancreatic exocrine secretion and gallbladder contraction. NPYY, an appetite stimulator, is produced by gut endocrine cells, and is released post-prandially [16]. It is also a vasoconstrictor [5,16].

Glucagon-like peptide 1 (GLP-1) and oxyntomodulin

Both act as satiety signals. GLP-1 is cleaved from pro glucagon and released from the L-cells of the intestinal ileum and colon into the systemic circulation [5,20]. GLP-1 and its longer acting receptor agonists decrease food intake and have a strong incretin effect (increased stimulation of insulin) from oral glucose feeding [20,30]. Oxyntomodulin, also derived from pro glucagon, is co-secreted with GLP-1. It induces satiety, increases energy expenditure and decreases weight [5,20]. Both GLP-1 and oxyntomodulin are processed by the CNS, intestine and colon, and released in response to nutrient intake. They inhibit gastric acid secretion and reduce food intake [5,19,20]. Importantly, effective control of appetite expression remains a critical therapeutic target for weight management [1]. Current strategies utilize a combination of agents to target both homeostatic and hedonic control mechanisms [16,20].

Controlling Appetite

Leptin and 5-HT belong to separate systems for controlling appetite [28]. Satiation of hunger within and after meals is signaled by 5-HT in response to the pattern of an individual’s food intake [27,29]. Circulating levels of the 5-HT precursor amino acid, tryptophan, along with certain macronutrients and peripheral satiety factors such as CCK and enterostatin control CNS 5-HT output. Hypothalamic 5-HT receptor systems inhibit NPYY, which is a potent stimulator of hunger and food intake. The hormone leptin, by contrast, provides a signal linking the status of adipose tissue with a number of important CNS circuits. Leptin itself stimulates CNS leptin receptors, which link with proopiomelanocortin (POMC) and melanocortin 4 (MC-4) receptors, leading to hypephagia and obesity. The effects of leptin may also be modulated by factors such as the corticotrophin-releasing factor (CRF), cocaine and amphetamine-regulated transcript (CART), orexins and galanin [16]. These separate 5-HT and leptin systems act as short-acting satiety signals (episodic in nature), and as a hormonal indicator of long-term (tonic) energy reserves, respectively [28].

Several mechanisms have been identified whereby certain pharmacological agents can induce changes in food intake, body weight and eventually in body composition [1]. Some of these drugs modify the appetite system as measured by subjective changes in feelings of hunger and fullness (indices of satiety), and are considered to be “appetite suppressants”. Appetite suppressants act either via peripheral satiety peptide systems (such as CCK and enterostatin), or by altering CNS levels of various hypothalamic neuro peptides (NPYY, galanin, orexin and MC-4) or by changing levels of the key CNS appetite neurotransmitters such as 5-HT and noradrenaline [1].


Both human and companion animal populations are facing increasing problems associated with weight gain and obesity. The control of appetite, also known as the appestat, requires a balanced interplay between the brain, digestive tract and adipose tissue, and is tightly regulated by the hypothalamus. The primary fat regulating hormones are adiponectin, serotonin, leptin and ghrelin. While the human and animal body also have so-called “obesity genes”, the determining factors are most often related to their shared common environment and individual lifestyles. The future success of appetite control for humans and pet animals will depend upon use of effective targeted pharmacological agents in conjunction with dietary modification (less high glycemic carbohydrates and fat) and lifestyle changes (more exercise).


1. Halford JC, Blundell JE. Pharmacology of appetite suppression. Prog Drug Res. 2000; 54: 25-58.

2. Dodds WJ, Laverdure, DR. Canine Nutrigenomics: The New Science of Feeding Your Dog for Optimal Health, Dog Wise. 2015; 315.

3. German AJ. The growing problem of obesity in dogs and cats. J Nutr. 2006; 136: 1940S-1946S.

4. Association for Pet Obesity Prevention. National Pet Obesity Survey Results. 2012.

5. Yu JH, Kim MS. Molecular mechanisms of appetite regulation. Diabetes Metab J. 2012; 36: 391-398.

6. Banfield Pet Hospital. State of Pet Health. 2012.

7. Ley RE, Hamady M, Lozupone C, Turnbaugh PJ, Ramey RR, Bircher JS, et al. Evolution of mammals and their gut microbes. Science. 2008; 320: 1647-1651.

8. Bäckhed F, Ley RE, Sonnenburg JL, Peterson DA, Gordon JI. Hostbacterial mutualism in the human intestine. Science. 2005; 307: 1915- 1920.

9. Ollivier M, Tresset A, Bastian F, Lagoutte L, Axelsson E, Arendt ML, et al. Amy2B copy number variation reveals starch diet adaptations in ancient European dogs. R Soc Open Sci. 2016; 3: 160449.

10.Diaz Heijtz R, Wang S, Anuar F, Qian Y, Björkholm B, Samuelsson A, et al. Normal gut microbiota modulates brain development and behavior. Proc Natl Acad Sci U S A. 2011; 108: 3047-3052.

11.Song SJ, Lauber C, Costello EK, Lozupone CA, Humphrey G, Berg0Lyons D, et al. Cohabiting family members share microbiota with one another and with their dogs. Life. 2013; 2: e00458.

12.Ley RE1, Bäckhed F, Turnbaugh P, Lozupone CA, Knight RD, Gordon JI. Obesity alters gut microbial ecology. Proc Natl Acad Sci U S A. 2005; 102: 11070-11075.

13.Tehrani AB, Nezami BG, Gewirtz A, Srinivasan S. Obesity and its associated disease: a role for microbiota? Neurogastroenterol Motil. 2012; 24: 305-311.

14.Rui L. Brain regulation of energy balance and body weight. Rev Endocr Metab Disord. 2013; 14: 387-407.

15.Harrold JA, Dovey TM, Blundell JE, Halford JC. CNS regulation of appetite. Neuropharmacology. 2012; 63: 3-17.

16.Ahima RS, Antwi DA. Brain regulation of appetite and satiety. Endocrinol Metab Clin North Am. 2008; 37: 811-823.

17.Jones MP, Dilley JB, Drossman D, Crwell MD. Brain-gut connections in functional GI disorders: Anatomic and physiologic relationships. Neurogastroent Motil. 2006; 18: 91-103.

18.Watts J. Appetite control & maintaining constant body weight. Vet Sci. 2010.

19.Murphy KG, Bloom SR. Gut hormones in the control of appetite. Exp Physiol. 2004; 89: 507-516.

20.De Vadder F, Mithieux G. Glucose homeostasis and gut-brain connection. Med Sci (Paris). 2015; 31: 168-173.

21.Klok MD, Jakobsdottir S, Drent ML. The role of leptin and ghrelin in the regulation of food intake and body weight in humans: a review. Obes Rev. 2007; 8: 21-34.

22.Schwartz GJ. The role of gastrointestinal vagal afferents in the control of food intake: current prospects. Nutrition. 2000; 16: 866-873.

23.De Lartigue G, dela Serre CB, Raybould HE. Vagal afferent neurons in high fat diet-induced obesity; intestinal microflora, gut inflammation and cholecystokinin. Physiol Behav. 2011; 105:100-105.

24.Cao H. Adipocytokines in obesity and metabolic disease. J Endocrinol. 2014; 220: T47-59.

25.Eisele I, Wood IS, German AJ, Hunter L, Trayhurn R. Adipokine gene expression in dog adipose tissues and dog white cell adipocytes differentiated in primary culture. Hormone Metabol Res. 2005; 37: 474-481.

26.Park HJ, Lee SE, Kim HB, Isaacson RE, Seo KW, Song KH. Association of obesity with serum leptin, adiponectin, and serotonin and gut microflora in beagle dogs. J Vet Intern Med. 2015; 29: 43-50.

27.Sharma S, Sharma J. Regulation of appetite: role of serotonin and hypothalamus. Iranian J Pharmacol & Therapeutics. 2012; 11: 73-79.

28.Halford JC, Blundell JE. Separate systems for serotonin and leptin in appetite control. Ann Med. 2000; 32: 222-232.

29.Stunes AK, Reseland JE, Hauso O, Kidd M, Tømmerås K, Waldum HL, et al. Adipocytes express a functional system for serotonin synthesis, reuptake and receptor activation. Diabetes Obes Metab. 2011; 13: 551-558.

30.Jéquier E. Leptin signaling, adiposity, and energy balance. Ann N Y Acad Sci. 2002; 967: 379-388.

31.Simpson KA, Martin NM, Bloom SR. Hypothalamic regulation of appetite. Expert Rev Endocrinol Metab. 2008; 3: 577-592.

32.Yamka RM, Friesen KG, Gao X, Malladi S, Al-Murrani S. Identification of genes related to obesity in dogs. The FASEB J. 2007; 21: 28.4.

33.Yamka RM, Frantz NZ, Friesen KG. Effects of 3 canine weight loss foods on body composition and obesity markers. Int J Applied Res Vet Med. 2007; 5: 125-132.

34.Kettner NM, Mayo SA, Hua J, Lee C, Moore DD, Fu L. Circadian Dysfunction Induces Leptin Resistance in Mice. Cell Metab. 2015; 22: 448-459.

Dodds WJ (2017) Central Nervous System Regulation of Appetite in Humans and Pet Animals. Ann Clin Exp Metabol 2(1): 1013

Received : 08 Sep 2016
Accepted : 07 Jan 2017
Published : 11 Jan 2017
Annals of Otolaryngology and Rhinology
ISSN : 2379-948X
Launched : 2014
JSM Schizophrenia
Launched : 2016
Journal of Nausea
Launched : 2020
JSM Internal Medicine
Launched : 2016
JSM Hepatitis
Launched : 2016
JSM Oro Facial Surgeries
ISSN : 2578-3211
Launched : 2016
Journal of Human Nutrition and Food Science
ISSN : 2333-6706
Launched : 2013
JSM Regenerative Medicine and Bioengineering
ISSN : 2379-0490
Launched : 2013
JSM Spine
ISSN : 2578-3181
Launched : 2016
Archives of Palliative Care
ISSN : 2573-1165
Launched : 2016
JSM Nutritional Disorders
ISSN : 2578-3203
Launched : 2017
Annals of Neurodegenerative Disorders
ISSN : 2476-2032
Launched : 2016
Journal of Fever
ISSN : 2641-7782
Launched : 2017
JSM Bone Marrow Research
ISSN : 2578-3351
Launched : 2016
JSM Mathematics and Statistics
ISSN : 2578-3173
Launched : 2014
Journal of Autoimmunity and Research
ISSN : 2573-1173
Launched : 2014
JSM Arthritis
ISSN : 2475-9155
Launched : 2016
JSM Head and Neck Cancer-Cases and Reviews
ISSN : 2573-1610
Launched : 2016
JSM General Surgery Cases and Images
ISSN : 2573-1564
Launched : 2016
JSM Anatomy and Physiology
ISSN : 2573-1262
Launched : 2016
JSM Dental Surgery
ISSN : 2573-1548
Launched : 2016
Annals of Emergency Surgery
ISSN : 2573-1017
Launched : 2016
Annals of Mens Health and Wellness
ISSN : 2641-7707
Launched : 2017
Journal of Preventive Medicine and Health Care
ISSN : 2576-0084
Launched : 2018
Journal of Chronic Diseases and Management
ISSN : 2573-1300
Launched : 2016
Annals of Vaccines and Immunization
ISSN : 2378-9379
Launched : 2014
JSM Heart Surgery Cases and Images
ISSN : 2578-3157
Launched : 2016
Annals of Reproductive Medicine and Treatment
ISSN : 2573-1092
Launched : 2016
JSM Brain Science
ISSN : 2573-1289
Launched : 2016
JSM Biomarkers
ISSN : 2578-3815
Launched : 2014
JSM Biology
ISSN : 2475-9392
Launched : 2016
Archives of Stem Cell and Research
ISSN : 2578-3580
Launched : 2014
Annals of Clinical and Medical Microbiology
ISSN : 2578-3629
Launched : 2014
JSM Pediatric Surgery
ISSN : 2578-3149
Launched : 2017
Journal of Memory Disorder and Rehabilitation
ISSN : 2578-319X
Launched : 2016
JSM Tropical Medicine and Research
ISSN : 2578-3165
Launched : 2016
JSM Head and Face Medicine
ISSN : 2578-3793
Launched : 2016
JSM Cardiothoracic Surgery
ISSN : 2573-1297
Launched : 2016
JSM Bone and Joint Diseases
ISSN : 2578-3351
Launched : 2017
JSM Bioavailability and Bioequivalence
ISSN : 2641-7812
Launched : 2017
JSM Atherosclerosis
ISSN : 2573-1270
Launched : 2016
Journal of Genitourinary Disorders
ISSN : 2641-7790
Launched : 2017
Journal of Fractures and Sprains
ISSN : 2578-3831
Launched : 2016
Journal of Autism and Epilepsy
ISSN : 2641-7774
Launched : 2016
Annals of Marine Biology and Research
ISSN : 2573-105X
Launched : 2014
JSM Health Education & Primary Health Care
ISSN : 2578-3777
Launched : 2016
JSM Communication Disorders
ISSN : 2578-3807
Launched : 2016
Annals of Musculoskeletal Disorders
ISSN : 2578-3599
Launched : 2016
Annals of Virology and Research
ISSN : 2573-1122
Launched : 2014
JSM Renal Medicine
ISSN : 2573-1637
Launched : 2016
Journal of Muscle Health
ISSN : 2578-3823
Launched : 2016
JSM Genetics and Genomics
ISSN : 2334-1823
Launched : 2013
JSM Anxiety and Depression
ISSN : 2475-9139
Launched : 2016
Clinical Journal of Heart Diseases
ISSN : 2641-7766
Launched : 2016
Annals of Medicinal Chemistry and Research
ISSN : 2378-9336
Launched : 2014
JSM Pain and Management
ISSN : 2578-3378
Launched : 2016
JSM Women's Health
ISSN : 2578-3696
Launched : 2016
Clinical Research in HIV or AIDS
ISSN : 2374-0094
Launched : 2013
Journal of Endocrinology, Diabetes and Obesity
ISSN : 2333-6692
Launched : 2013
Journal of Substance Abuse and Alcoholism
ISSN : 2373-9363
Launched : 2013
JSM Neurosurgery and Spine
ISSN : 2373-9479
Launched : 2013
Journal of Liver and Clinical Research
ISSN : 2379-0830
Launched : 2014
Journal of Drug Design and Research
ISSN : 2379-089X
Launched : 2014
JSM Clinical Oncology and Research
ISSN : 2373-938X
Launched : 2013
JSM Bioinformatics, Genomics and Proteomics
ISSN : 2576-1102
Launched : 2014
JSM Chemistry
ISSN : 2334-1831
Launched : 2013
Journal of Trauma and Care
ISSN : 2573-1246
Launched : 2014
JSM Surgical Oncology and Research
ISSN : 2578-3688
Launched : 2016
Annals of Food Processing and Preservation
ISSN : 2573-1033
Launched : 2016
Journal of Radiology and Radiation Therapy
ISSN : 2333-7095
Launched : 2013
JSM Physical Medicine and Rehabilitation
ISSN : 2578-3572
Launched : 2016
Annals of Clinical Pathology
ISSN : 2373-9282
Launched : 2013
Annals of Cardiovascular Diseases
ISSN : 2641-7731
Launched : 2016
Journal of Behavior
ISSN : 2576-0076
Launched : 2016
Clinical Research in Infectious Diseases
ISSN : 2379-0636
Launched : 2013
JSM Microbiology
ISSN : 2333-6455
Launched : 2013
Journal of Urology and Research
ISSN : 2379-951X
Launched : 2014
Journal of Family Medicine and Community Health
ISSN : 2379-0547
Launched : 2013
Annals of Pregnancy and Care
ISSN : 2578-336X
Launched : 2017
JSM Cell and Developmental Biology
ISSN : 2379-061X
Launched : 2013
Annals of Aquaculture and Research
ISSN : 2379-0881
Launched : 2014
Clinical Research in Pulmonology
ISSN : 2333-6625
Launched : 2013
Journal of Immunology and Clinical Research
ISSN : 2333-6714
Launched : 2013
Annals of Forensic Research and Analysis
ISSN : 2378-9476
Launched : 2014
JSM Biochemistry and Molecular Biology
ISSN : 2333-7109
Launched : 2013
Annals of Breast Cancer Research
ISSN : 2641-7685
Launched : 2016
Annals of Gerontology and Geriatric Research
ISSN : 2378-9409
Launched : 2014
Journal of Sleep Medicine and Disorders
ISSN : 2379-0822
Launched : 2014
JSM Burns and Trauma
ISSN : 2475-9406
Launched : 2016
Chemical Engineering and Process Techniques
ISSN : 2333-6633
Launched : 2013
Annals of Clinical Cytology and Pathology
ISSN : 2475-9430
Launched : 2014
JSM Allergy and Asthma
ISSN : 2573-1254
Launched : 2016
Journal of Neurological Disorders and Stroke
ISSN : 2334-2307
Launched : 2013
Annals of Sports Medicine and Research
ISSN : 2379-0571
Launched : 2014
JSM Sexual Medicine
ISSN : 2578-3718
Launched : 2016
Annals of Vascular Medicine and Research
ISSN : 2378-9344
Launched : 2014
JSM Biotechnology and Biomedical Engineering
ISSN : 2333-7117
Launched : 2013
Journal of Hematology and Transfusion
ISSN : 2333-6684
Launched : 2013
JSM Environmental Science and Ecology
ISSN : 2333-7141
Launched : 2013
Journal of Cardiology and Clinical Research
ISSN : 2333-6676
Launched : 2013
JSM Nanotechnology and Nanomedicine
ISSN : 2334-1815
Launched : 2013
Journal of Ear, Nose and Throat Disorders
ISSN : 2475-9473
Launched : 2016
JSM Ophthalmology
ISSN : 2333-6447
Launched : 2013
Journal of Pharmacology and Clinical Toxicology
ISSN : 2333-7079
Launched : 2013
Annals of Psychiatry and Mental Health
ISSN : 2374-0124
Launched : 2013
Medical Journal of Obstetrics and Gynecology
ISSN : 2333-6439
Launched : 2013
Annals of Pediatrics and Child Health
ISSN : 2373-9312
Launched : 2013
JSM Clinical Pharmaceutics
ISSN : 2379-9498
Launched : 2014
JSM Foot and Ankle
ISSN : 2475-9112
Launched : 2016
JSM Alzheimer's Disease and Related Dementia
ISSN : 2378-9565
Launched : 2014
Journal of Addiction Medicine and Therapy
ISSN : 2333-665X
Launched : 2013
Journal of Veterinary Medicine and Research
ISSN : 2378-931X
Launched : 2013
Annals of Public Health and Research
ISSN : 2378-9328
Launched : 2014
Annals of Orthopedics and Rheumatology
ISSN : 2373-9290
Launched : 2013
Journal of Clinical Nephrology and Research
ISSN : 2379-0652
Launched : 2014
Annals of Community Medicine and Practice
ISSN : 2475-9465
Launched : 2014
Annals of Biometrics and Biostatistics
ISSN : 2374-0116
Launched : 2013
JSM Clinical Case Reports
ISSN : 2373-9819
Launched : 2013
Journal of Cancer Biology and Research
ISSN : 2373-9436
Launched : 2013
Journal of Surgery and Transplantation Science
ISSN : 2379-0911
Launched : 2013
Journal of Dermatology and Clinical Research
ISSN : 2373-9371
Launched : 2013
JSM Gastroenterology and Hepatology
ISSN : 2373-9487
Launched : 2013
Annals of Nursing and Practice
ISSN : 2379-9501
Launched : 2014
JSM Dentistry
ISSN : 2333-7133
Launched : 2013
Author Information X