About

Dipak K. Sarkar is a Distinguished Professor and the Director of the Endocrine Program at Rutgers University, within the Department of Animal Sciences. His current research focuses on understanding how fetal alcohol exposures alter neuroimmune communications in the hypothalamus through extravesicular and epigenetic mechanisms, leading to stress hyper-response, behavioral abnormalities, metabolic dysfunctions, immune incompetence, and cancer. His scientific projects include studying signal transduction pathways for alcohol action on neuronal differentiation and neurotransmission, interactions between alcohol and opioid peptides in controlling natural killer cell activity, regulation of neuroendocrine and immune functions by clock genes, and the effects of fetal alcohol on stress axes and circadian rhythms. Additionally, his work explores neuronal stem cell differentiation, beta-endorphin cell transplants for stress and cancer control, alcohol-induced oxidative stress in developing neurons, epigenetic effects of alcohol on stress axis development, opioid receptor dimerization, neuron-glial interactions in controlling alcohol-induced apoptosis, and cell communication in hormonal carcinogenesis and pituitary tumor treatment. Dr. Sarkar has held various academic and research positions, including Chair and Professor at Rutgers, Director of the Alcohol and Drug Abuse Program at Washington State University, and faculty roles at the University of California, San Diego, Michigan State University, Yale University, and Oxford University. His educational background includes a D. Phil. from Oxford University and a Ph.D., M.S., and B.S. from Calcutta University. His extensive research experience and leadership in neuroendocrinology and alcohol studies underscore his contributions to understanding the biological impacts of alcohol and neuroimmune interactions.

Research topics

• Immunology
• Endocrinology
• Medicine
• Internal medicine
• Biology
• Cell biology
• Pharmacology
• Chemistry
• Biochemistry
• Genetics
• Andrology
• Cancer research
• Physiology

Selected publications

• Surgical approach towards cystorrhexis of a non-descript male calf- A case report

  Indian Journal of Animal Health · 2025-04-10

  articleOpen access

  The case was represented as a 6-month-old Indian non-descript male calf with a chief complaint of anuria with a distended abdomen for 48 hours.Clinical examination revealed fluid thrill on ballottement of ventro-lateral aspect of abdominal cavity.Moreover, abdominocentesis was done under aseptic conditions, indicating the fluid that resembled urine.The case was assumed to be cystorrhexis, which may have occurred due to obstructive urolithiasis, finally resulting into uroperitoneum.Surgical intervention involved cystorrhaphy and tube cystotomy with Foley's catheter through ventral paramedian site.Administration of supportive medications like appropriate choice of fluid to correct electrolyte and acid-base balance, especially for preventing shock, one broad spectrum antibiotic, anti-inflammatory drug, urinary acidifier and cellulolytic agent like ammonium chloride to the animal in the post-operative days.The calf was recovered after 2 weeks of surgery without any complications.

  PublisherDOI

• Prenatal alcohol exposure increases the aggressiveness of estrogen‐induced pituitary tumors in male rats

  Alcohol Clinical and Experimental Research · 2025-09-29

  articleOpen accessSenior author

  BACKGROUND: We have recently shown that estrogen-induced prolactin-secreting pituitary tumors are aggressive in prenatal alcohol-exposed female rats. In this study, we investigated whether similar tumor aggressiveness occurs in estrogen-treated prenatal alcohol-exposed male rats. METHODS: Pregnant Fischer 344 rats were fed from gestational days 7 and 21 with a liquid diet containing ethanol 6.7% v/v (AF), pair-fed with an isocaloric liquid diet (PF), or fed chow ad libitum (AD). Alcohol-fed dams exhibited a blood alcohol concentration of 120-150 mg/dL 2 h after the last feeding. Male offspring were orchiectomized at 60 days of age and implanted subcutaneously with estradiol implants. Four months after the estradiol implants, rats were sacrificed, and pituitary tumor tissues were collected. Tumor cells were isolated and cultured for analysis. RESULTS: Pituitary tumor cells from AF males exhibited stem-like cell properties and showed elevated expression of stem cell regulatory genes and proteins (SOX-2, OCT-4, KLF4, SNAIL-1, and Nestin), tumor aggressiveness markers (MMP-9, CD44, CD34, PTTG, FGFR4, Ki-67, N-Cadherin), and prolactin compared to those from AD and PF controls. AF cells also had a higher cell proliferation rate, increased invasiveness, and colony formation compared to those in AD and PF cells, indicating more aggressive cancer cells than control cells. Notably, AF cells had a higher expression of developmental pluripotency-associated 4 (Dppa4), a gene we recently identified as upregulated in aggressive tumors and in fetal alcohol-exposed animals. CONCLUSIONS: These findings are consistent with our previous observations in estrogen-treated AF female rats. These results support the hypothesis that prenatal alcohol exposure programs the pituitary epithelium toward a mesenchymal stem cell-like phenotype, contributing to the development of aggressive pituitary prolactinomas in both sexes.

  PublisherDOI

• Prenatal alcohol exposure induces microglia to release exosomes with an elevated level of MIP-1α that participates in apoptotic process of stress-regulatory proopiomelanocortin neurons via glutamate excitotoxicity

  Brain Behavior and Immunity · 2025-07-19

  articleSenior authorCorresponding
  PublisherDOI

• Surgical management of a compound tibiotarsus fracture in a rose-ringed parakeet (Psittacula krameri) - A case report

  Indian Journal of Animal Health · 2025-05-26

  articleOpen access

  A 2-year-old Rose-Ringed Parakeet was presented with a history of physical trauma.On physical examination, it was revealed a compound fracture of the right tibia.The fracture was reduced and stabilized by the application of intra medullary 18 G sutureless stainless steel surgical needle, in a retrograde manner.Modified Robert Jones along with a splint was applied as protective bandage.Post-operatively the antibiotic and analgesic were advised.The bird was assessed for recovery by physical and radiographic evaluation after 2 months of surgery.The X-rays showed good callus accumulation and healing of the fractured part, and the bird regained its normal gait.Hence, it is concluded that the use of a stainless-steel needle corresponding to the required size is an effective and successful immobilization process in the tibiotarsus fracture repair of a parakeet.

  PublisherDOI

• Developmental pluripotency-associated 4 increases aggressiveness of pituitary neuroendocrine tumors by enhancing cell stemness

  Neuro-Oncology · 2024-08-02 · 7 citations

  articleOpen accessSenior authorCorresponding

  BACKGROUND: Pituitary neuroendocrine tumors, PitNETs, are often aggressive and precipitate in distant metastases that are refractory to current therapies. However, the molecular mechanism in PitNETs' aggressiveness is not well understood. Developmental pluripotency-associated 4 (DPPA4) is known as a stem cell regulatory gene and overexpressed in certain cancers, but its function in the context of PitNETs' aggressiveness is not known. METHODS: We employed both rat and human models of PitNETs. In the rat pituitary tumor model, we used prenatal-alcohol-exposed (PAE) female Fischer rats which developed aggressive PitNETs following estrogen treatment, while in the human pituitary tumor model, we used aggressively proliferative cells from pituitary tumors of patients undergone surgery. Various molecular, cellular, and epigenetic techniques were used to determine the role of DPPA4 in PitNETs' aggressiveness. RESULTS: We show that DPPA4 is overexpressed in association with increased cell stemness factors in aggressive PitNETs of PAE rats and of human patients. Gene-editing experiments demonstrate that DPPA4 increases the expression of cell stemness and tumor aggressiveness genes and promotes proliferation, colonization, migration, and tumorigenic potential of PitNET cells. ChIP assays and receptor antagonism studies reveal that DPPA4 binds to canonical WINTs promoters and increases directly or indirectly the WNT/β-CATENIN control of cell stemness, tumor growth, and aggressiveness of PitNETs. Epigenetic studies show the involvement of histone methyltransferase in alcohol activation of DPPA4. CONCLUSIONS: These findings support a role of DPPA4 in tumor stemness and aggressiveness and provide a preclinical rationale for modulating this stemness regulator for the treatment of PitNETs.

  PublisherOA PDFDOI

• Altered circadian expression of clock genes and clock-regulatory epigenetic modifiers in saliva of children with fetal alcohol spectrum disorders

  Scientific Reports · 2024-08-27 · 5 citations

  articleOpen accessSenior author

  Prenatal alcohol-exposed (AE) infants and children often demonstrate disrupted sleep patterns, including more frequent awakenings, reduced total sleep time, and more night-to-night sleep variability. Despite the strong connection between sleep patterns and circadian rhythmicity, relatively little is known about circadian rhythm disruptions in individuals with AE. Recently, several reports demonstrated that evaluating the expression patterns of human clock genes in biological fluids could reveal an individual's circadian phenotype. Human saliva offers an emerging and easily available physiological sample that can be collected non-invasively for core-clock gene transcript analyses. We compared the expression patterns of core-clock genes and their regulatory genes in salivary samples of children aged 6-10 years-old with and without AE during the light cycle between ZT0-ZT11. We isolated the RNA from the samples and measured the expression patterns of core clock genes and clock regulating genes using the human specific primers with quantitative real-time PCR. Analysis of core clock genes expression levels in saliva samples from AE children indicates significantly altered levels in expression of core-clock BMAL1, CLOCK, PER1-3 and CRY1,2, as compared to those in age-matched control children. We did not find any sex difference in levels of clock genes in AE and control groups. Cosinor analysis was used to evaluate the rhythmic pattern of these clock genes, which identified circadian patterns in the levels of core clock genes in the control group but absent in the AE group. The gene expression profile of a salivary circadian biomarker ARRB1 was rhythmic in saliva of control children but was arhythmic in AE children. Altered expression patterns were also observed in clock regulatory genes: NPAS2, NFL3, NR1D1, DEC1, DEC2, and DBP, as well as chromatin modifiers: MLL1, P300, SIRT1, EZH2, HDAC3, and ZR1D1, known to maintain rhythmic expression of core-clock genes. Overall, these findings provide the first evidence that AE disturbs the circadian patten expression of core clock genes and clock-regulatory chromatin modifiers in saliva.

  PublisherOA PDFDOI

• Ethanol-activated microglial exosomes induce MCP1 signaling mediated death of stress-regulatory proopiomelanocortin neurons in the developing hypothalamus

  Journal of Neuroinflammation · 2024-10-30 · 5 citations

  articleOpen accessSenior author

  BACKGROUND: Microglia, a type of resident immune cells within the central nervous system, have been implicated in ethanol-activated neuronal death of the stress regulatory proopiomelanocortin (POMC) neuron-producing β-endorphin peptides in the hypothalamus in a postnatal rat model of fetal alcohol spectrum disorders. We determined if microglial extracellular vesicles (exosomes) are involved in the ethanol-induced neuronal death of the β-endorphin neuron via secreting elevated levels of the chemokine monocyte chemoattractant protein 1 (MCP1), a key regulator of neuroinflammation. METHODS: We employed an in vitro model, consisting of primary culture of hypothalamic microglia prepared from postnatal day 2 (PND2) rat hypothalami and treated with or without 50 mM ethanol for 24 h, and an in vivo animal model in which microglia were obtained from hypothalami of PND6 rats fed daily with 2.5 mg/kg ethanol or control milk formula for five days prior to use. Exosomes were extracted and characterized with nanosight tracking analysis (NTA), transmission electron microscopy and western blot. Chemokine multiplex immunoassay and ELISA were used for quantitative estimation of MCP1 level. Neurotoxic ability of exosome was tested using primary cultures of β-endorphin neurons and employing nucleosome assay and immunocytochemistry. Elevated plus maze, open field and restraint tests were used to assess anxiety-related behaviors. RESULTS: Ethanol elevated MCP1 levels in microglial exosomes both in vitro and in vivo models. Ethanol-activated microglial exosomes when introduced into primary cultures of β-endorphin neurons, increased cellular levels of MCP1 and the chemokine receptor CCR2 related signaling molecules including inflammatory cytokines and apoptotic genes as well as apoptotic death of β-endorphin neurons. These effects of microglial exosomes on β-endorphin neurons were suppressed by a CCR2 antagonist RS504393. Furthermore, RS504393 when injected in postnatal rats prior to feeding with ethanol it reduced alcohol-induced β-endorphin neuronal death in the hypothalamus. RS504393 also suppressed corticosterone response to stress and anxiety-like behaviors in postnatally alcohol-fed rats during adult period. CONCLUSION: These data suggest that alcohol exposures during the developmental period elevates MCP1 levels in microglial exosomes that promote MCP1/CCR2 signaling to increase the apoptosis of β-endorphin neurons and resulting in hormonal and behavioral stress responses.

  PublisherOA PDFDOI

• Exploring the intersection of polygenic risk scores and prenatal alcohol exposure: Unraveling the mental health equation

  Alcohol Clinical and Experimental Research · 2024-09-29 · 1 citations

  articleOpen accessSenior authorCorresponding

  Abstract Background Prenatal alcohol exposure poses significant risks to offspring mental health. However, the interplay between genetic predispositions to mental health disorders and prenatal alcohol exposure remains incompletely understood, limiting our ability to develop effective interventions for these conditions. Methods Data from the Adolescent Brain and Cognitive Development (ABCD) Study were analyzed to explore associations between polygenic risk scores (PRS) for mental disorders and maternal alcohol consumption during pregnancy. Logistic regression and structural equation modeling were utilized to assess these relationships. Results Maternal alcohol consumption after pregnancy awareness was significantly associated with an increased genetic risk for specific mental health disorders, particularly bipolar disorder in offspring. The relationship between maternal alcohol consumption and mental health outcomes was influenced by polygenic risk scores, with both externalizing and internalizing problems being affected. Conclusions Our findings highlight the specific interaction between increased genetic risk for bipolar disorder and prenatal alcohol exposure in shaping offspring mental health outcomes. The significant associations we observed underscore the importance of considering both polygenic risk scores and prenatal alcohol exposure when assessing mental health risks in children. These insights emphasize the need for targeted interventions that address both genetic predispositions and environmental exposures to better understand and mitigate the impact on offspring mental health.

  PublisherOA PDFDOI

• Supplemental Figure 4 from Beta-Endorphin Cell Therapy for Cancer Prevention

  2023-04-03

  preprintOpen accessSenior author

  <p>SFigure 4: Representative photomicrograph of a section of rat brain showing fluorescently-labeled-nanosphere attached with cAMP (N-cAMP; blue) in the area of 3rd ventricle.</p>

  PublisherDOI

• Supplementary Figure 2 from Beta-Endorphin Cell Therapy for Cancer Prevention

  2023-04-03

  preprintOpen accessSenior author

  <p>SFigure 2: Representative picture of a back tumor, which developed in some control neuron transplanted animals following intravenous injection of MADB106 cells in female F344 rats.</p>

  PublisherDOI

Recent grants

• NIH Grant R01HL088041

  NIH · $817k · 2011

• Rates of histone turnover and functional significance in fetal alcohol syndrome

  NIH · $409k · 2016–2019

• NIH Grant K02AA000220

  NIH · $493k · 2002

• NIH Grant R01AA015718

  NIH · $1.6M · 2012

• NIH Grant R01CA077500

  NIH · $801k · 2005

Frequent coauthors

• Nadka Boyadjieva

  91 shared

• Sengottuvelan Murugan

  35 shared

• Keith W. Singletary

  Goodwin College

  32 shared

• Joachim G. Liehr

  Christus Stehlin Foundation for Cancer Research

  32 shared

• Changqing Zhang

  Shanghai Jiao Tong University

  32 shared

• Shaima Jabbar

  Rutgers, The State University of New Jersey

  28 shared

• Karen M. Tobias

  25 shared

• Ruth C. Newberry

  Norwegian University of Life Sciences

  25 shared

Education

• DPhil, Human Anatomy

  University of Oxford

  1979

Awards & honors

• Distinguished Professor and Director - Endocrine Program, Ce…
• Chair and Professor - Dept. of Animal Sciences, Rutgers Univ…
• Director - Alcohol and Drug Abuse Program, Washington State…
• Adjunct Professor - Department of Genetics and Cell Biology,…
• Adjunct Professor - Program of Pharmacology and Toxicology,…