Anjali Varma
· ProfessorVirginia Tech · Psychiatry and Behavioral Medicine
Active 1996–2024
Research topics
- Biochemistry
- Biophysics
- Cell biology
- Surgery
- Endocrinology
- Ecology
- Chromatography
- Chemistry
- Biology
- Medicine
Selected publications
Why Parental Education may be the Key to Raising the Digital Natives?
Indian Pediatrics · 2024
1st authorCorresponding- Medicine
- Surgery
- Ecology
Molecular and Cellular Endocrinology · 2024
- Chemistry
- Cell biology
- Biochemistry
Insulin is an important regulator of whole-body glucose homeostasis. In insulin sensitive tissues such as muscle and adipose, insulin induces the translocation of glucose transporter 4 (GLUT4) to the cell membrane, thereby increasing glucose uptake. However, insulin also signals in tissues that are not generally associated with glucose homeostasis. In the human reproductive endocrine axis, hyperinsulinemia suppresses the secretion of gonadotropins from gonadotrope cells of the anterior pituitary, thereby linking insulin dysregulation to suboptimal reproductive health. In the mouse, gonadotropes express the insulin receptor which has the canonical signaling response of IRS, AKT, and mTOR activation. However, the functional outcomes of insulin action on gonadotropes are unclear. Here, we demonstrate through use of an optimized cell fractionation protocol that insulin stimulation of the LβT2 gonadotropic cell line results in the unexpected translocation of GLUT1 to the plasma membrane. Using our high purity fractionation protocol, we further demonstrate that though Akt signaling in response to insulin is intact, insulin-induced translocation of GLUT1 occurs independently of Akt activation in LβT2 cells.
Impact of opioid therapy on gonadal hormones: focus on buprenorphine
Hormone Molecular Biology and Clinical Investigation · 2018-02-17 · 14 citations
review1st authorCorrespondingObjective The USA is in the midst of an opioid crisis. Understanding the impact of opioids and commonly used treatments for opioid dependence is essential for clinicians and researchers in order to educate and treat the nation's growing population with opioid use disorders. As a relatively new treatment for opioid dependence, buprenorphine is gaining popularity to the extent of becoming not only a preferred approach to the maintenance of opiate addiction, but also an option for chronic pain management. The purpose of this report is to review the available evidence on the endocrine effects of buprenorphine, particularly as it relates to the hypothalamic-pituitary-gonadal (HPG) axis, which is controversial and not fully defined. Method We conducted a Pubmed search (2000-2017) for human studies in the English language for articles that were available as full length regarding buprenorphine, endocrinopathy, hypogonadism, bone density, opioids. Case reports were also reviewed, although prospective studies and randomized controlled trials received more weight. Results Opioid induced hypogonadism is well established. Most studies report that buprenorphine being a partial agonist/antagonist may not be impacting the pituitary trophic hormones as much. There are reports of sexual dysfunction in subjects maintained on buprenorphine, some without hormonal correlation. Thus with the understanding that pertinent clinical studies are limited in number, varied in methodology, mostly cross sectional, predominantly in men and small number of participants, more research in this area is warranted. Conclusion Based on a comprehensive review of the available literature, we conclude that despite its increasing popularity, buprenorphine has not been adequately studied in respect to its long-term effects on the hypothalamic-pituitary-adrenal (HPA) axis. There is a great need for longitudinal systematic trials to define the potential buprenorphine-induced endocrine consequences.
Journal of Alcoholism and Drug Dependence · 2017-01-01 · 2 citations
article1st authorCorrespondingBuprenorphine is a partial agonist at the mu opioid receptor. As compared to methadone, it has the advantage of being used in office based treatment setting, making this a preferred treatment option for opioid dependence. While opioid-induced urinary retention and hesitancy are well known, urinary hesitancy in patients who receive buprenorphine treatment may go unrecognized and untreated. Objectives: The current study is a retrospective chart review of 104 charts of patients with a diagnosis of opioid dependence who received buprenorphine/naloxone treatment to examine the incidence of urinary hesitancy and identify the relationship of symptoms, if any, with the dose and duration of treatment and other patient and treatment factors. Results: Forty-five percent of patients reported no side effects, while 26% of the subjects reported urinary hesitancy symptoms at some point in treatment. Urinary symptoms were reported as early as one day and predominantly in the first 2 weeks after initiation of bup/nlx treatment. Conclusion: Urinary hesitancy occurs with buprenorphine is often under reported and may go untreated. It may lead to significant discomfort and could possibly interfere with patient compliance to buprenorphine treatment. In most cases the symptoms are mild and transient and can easily be treated with increased fluid intake and use of bethanechol, a cholinergic drug that has long been used for non-obstructive urinary hesitancy or retention, at low doses. Education of providers and patients regarding this early and tr
Schizophrenia Research · 2016-06-15 · 32 citations
articleSenior authorAnti-NMDA Receptor Encephalitis: A Need for Increased Awareness Among Psychiatrists
Psychiatric Annals · 2015-11-01
article1st authorCorrespondingAnti–N-methyl-D-aspartate (NMDA) receptor encephalitis may present with a wide variety of early neuropsychiatric symptoms such as psychosis, insomnia, catatonia, and agitation, and at times in the absence of fever. The literature highlights the vital role of psychiatrists in early recognition and timely treatment of this condition. Presence of immunoglobulin G antibodies in blood and cerebrospinal fluid (CSF) against the NR1a subunit of the NMDA receptor is considered the gold standard for confirming diagnosis. There may be other nonspecific findings in CSF and on electroencephalogram and brain magnetic resonance imaging. Management includes surgical removal of the tumor if identified, first- and second-line immunotherapy, supportive medical care, and management of psychiatric symptoms. The role of electroconvulsive therapy has been noted for treatment of catatonic symptoms in particular. [ Psychiatr Ann . 2015;45(11):572–576.]
Low Testosterone Levels Associated With Venlafaxine Use
The Primary Care Companion For CNS Disorders · 2014-10-14 · 9 citations
articleSenior authorTo the Editor: Sexual dysfunction is a frequent side effect of selective serotonin reuptake inhibitors and serotonin-norepinephrine reuptake inhibitors. However, accompanying change in testosterone levels is uncommon. We present the case of a patient with posttraumatic stress disorder, major depressive disorder, and panic disorder, whose symptoms were well controlled with venlafaxine extended release 150 mg/day. Due to low testosterone levels, the venlafaxine treatment was tapered off. Case report. Mr A is a 36-year-old man with a history of major depressive disorder, posttraumatic stress disorder, and panic disorder. He presented to the mental health outpatient psychiatry clinic complaining of worsened anxiety, depression, and resumption of panic attacks after he was weaned off venlafaxine treatment 2 weeks earlier. Mr A had been depressed and suffering from anxiety for 18 months and started taking venlafaxine 14 months prior to his visit to the outpatient clinic. The taper began after Mr A presented to his primary care physician with fatigue, low sex drive, and weight gain, with inability to lose any weight despite a strict diet and exercise regimen. His total testosterone level taken at that time was 227 ng/dL (reference range, 241–827 ng/dL). Free testosterone levels were not taken and would not have added any significant insight to Mr A’s care, as level of total testosterone is sufficiently informative. The need for free testosterone levels is not crucial, as the bioavailability of albumin-bound testosterone is supported by evidence.1 Mr A’s luteinizing hormone and follicle-stimulating hormone levels were within normal limits. Over the course of 3 weeks, venlafaxine was tapered off by the primary care provider, assuming that venlafaxine was the cause of his low testosterone level. Mr A returned to the primary care provider for follow-up laboratory tests; his total testosterone level was 308 ng/dL. This result was reviewed by the endocrinology department in our outpatient clinic, and it was deemed unnecessary to give Mr A testosterone supplementation. Mr A was started on sertraline 50 mg/d but did not show up for follow-up appointments. He was contacted via phone and reported improvement in sexual function, as well as decreased symptoms of anxiety and depression. It is unclear if Mr A remained compliant with sertraline, as he no longer follows up in the outpatient psychiatry clinic. In reviewing the case, we found that Mr A had been a healthy adult with no preexisting medical conditions who was not taking steroids, opioids, or any other medications that would cause androgen disturbance or be a potential cause of low testosterone levels. There was no history of current or past illicit drug use such as heroin or prescription medication. His normal luteinizing hormone and follicle-stimulating hormone levels also confirmed that opioids were not the cause.2 Nonetheless, psychiatrists and primary care clinicians should be aware of drugs and medications that can potentially cause changes in testosterone levels and also that low testosterone levels may frequently mimic depression symptoms, such as low libido, anhedonia, fatigue, poor strength and energy with low appetite, and poor sleep. Some patients may also complain of anxiety symptoms. Unless clinicians are well aware and vigilant, such conditions may go unrecognized and untreated. There is very little literature on the relationship between venlafaxine and testosterone levels. We conducted a literature review and found a case report with similar results as those of Mr A. In the published case,3 a patient was found to have low testosterone levels, which returned to normal after venlafaxine discontinuation. With the exception of that case report, literature on the subject is lacking. This shortage of literature may be due to the rarity of this side effect, or it could be due to the lack of monitoring of testosterone levels in patients with symptoms closely resembling those of our patient. It is also worth mentioning that even healthy men may have fluctuating testosterone levels, and a low testosterone level may be transient.4 To the best of our knowledge, only one other case of low testosterone possibly linked to venlafaxine use has been reported.3 Although routine testosterone level tests are not warranted in all patients receiving venlafaxine, clinicians aware of this possible association may consider obtaining free and total testosterone levels before and after starting venlafaxine in select patient populations, such as those reporting low libido or fatigue. Since testosterone supplementation is not without its own adverse effects, supplementation may be considered on a case-by-case basis after discussion with endocrinologist colleagues.
Indian Pediatrics · 2014-05-01 · 11 citations
letterOpen accessPubMed · 2014-05-01 · 7 citations
editorial1st authorCorrespondingDeliberate self-harm in children- a growing problem
Indian Pediatrics · 2011-05-01
letter1st authorCorresponding
Frequent coauthors
- 17 shared
Mamta Sapra
Carilion Clinic
- 14 shared
Elizabeth Geras‐Raaka
National Institutes of Health
- 13 shared
John Moriarty
- 13 shared
Marvin C. Gershengorn
National Institutes of Health
- 13 shared
Michael Trimble
University College London
- 12 shared
Ali Iranmanesh
- 9 shared
J. M. Stevens
St Vincent’s Private Hospital Sydney
- 9 shared
Morgan Fish
West Virginia University
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