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Article ; Online: The Hypothalamic Melanocortin Pathway and the Regulation of Glucose Handling in the Kidney: A Sympathetic Look at Brain-Kidney Connection.

Obici, Silvana

2016 Volume 65, Issue 3, Page(s) 548–550

MeSH term(s)	Animals ; Arcuate Nucleus of Hypothalamus/metabolism ; Blood Glucose/metabolism ; Glucose Transporter Type 2/genetics ; Glycosuria, Renal/genetics ; Insulin Resistance/genetics ; Kidney/metabolism ; Obesity/genetics ; Pro-Opiomelanocortin/genetics ; Sympathetic Nervous System/metabolism
Chemical Substances	Blood Glucose ; Glucose Transporter Type 2 ; Pro-Opiomelanocortin (66796-54-1)
Language	English
Publishing date	2016-03
Publishing country	United States
Document type	Comment ; Journal Article
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/dbi15-0033
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Article: Radioiodine Therapy-Induced Conversion of Toxic Adenoma to Graves' Disease.

Rehman, Anis / Obici, Silvana / Yaqub, Abid

Cureus

2020 Volume 12, Issue 6, Page(s) e8683

Abstract: We present a 50-year-old female who was evaluated for the symptoms of thyrotoxicosis. She had low thyroid stimulating hormone (TSH) 0.02 with normal free thyroxine (FT4) 1.00 (0.61-1.76 ng/dL) and normal total triiodothyronine (TT3) 1.0 (0.60-2.20 ng/mL) ...

Abstract	We present a 50-year-old female who was evaluated for the symptoms of thyrotoxicosis. She had low thyroid stimulating hormone (TSH) 0.02 with normal free thyroxine (FT4) 1.00 (0.61-1.76 ng/dL) and normal total triiodothyronine (TT3) 1.0 (0.60-2.20 ng/mL) levels. Her thyrotropin receptor antibody (TRAbs) and thyroid peroxidase antibody (TPOAb) titers were negative. Thyroid ultrasound revealed an ill-defined, heterogeneous, 1.8 cm x 0.8 cm x 0.7 cm nodule in the left lower lobe. 123-radioiodine (RAI) thyroid scan revealed 38.5% uptake, which was concentrated in the lower left thyroid lobe, a finding consistent with a solitary toxic adenoma of the thyroid. The patient became clinically and biochemically euthyroid on methimazole (MMI). She then underwent 131-RAI therapy with 12 mCi, which cured her hyperthyroidism with normalization of TSH levels for four months. She then developed overt thyrotoxicosis with low TSH of 0.02, elevated TT3 of 3.2, and normal FT4 of 0.91. Repeat TRAbs and TPOAb were elevated along with diffusely increased uptake on the I-123 RAI thyroid uptake scan, consistent with Graves' disease (GD). The patient was then placed on MMI again to bridge to definitive treatment with total thyroidectomy. Our case is a rare case where the patient with solitary toxic adenoma with negative TPOAb serology developed GD following I-131 RAI treatment.
Language	English
Publishing date	2020-06-18
Publishing country	United States
Document type	Case Reports
ZDB-ID	2747273-5
ISSN	2168-8184
ISSN	2168-8184
DOI	10.7759/cureus.8683
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Article ; Online: How the hypothalamus controls glucose production: an update.

Prodi, Elena / Demuro, Giovanna / Obici, Silvana

Expert review of endocrinology & metabolism

2019 Volume 1, Issue 5, Page(s) 601–608

Abstract: Recent evidence highlights a crucial role of the brain in the control of glucose homeostasis. The hypothalamus senses and integrates signals of fuel abundance, such as circulating macronutrients (glucose and fatty acids) and nutrient-induced hormones ( ... ...

Abstract	Recent evidence highlights a crucial role of the brain in the control of glucose homeostasis. The hypothalamus senses and integrates signals of fuel abundance, such as circulating macronutrients (glucose and fatty acids) and nutrient-induced hormones (insulin and leptin). This, in turn, results in the activation of neural pathways that return circulating nutrients to baseline by reducing hepatic glucose production and food intake. In Type 2 diabetes and obesity, the ability of the brain to sense and respond to circulating signals is impaired. In this review, the neuroendocrine circuits that have recently been involved in the regulation of endogenous glucose production in rodents will be described. The study of these neural pathways promises to unveil new targets for the therapy of Type 2 diabetes and obesity.
Language	English
Publishing date	2019-02-12
Publishing country	England
Document type	Journal Article
ISSN	1744-8417
ISSN (online)	1744-8417
DOI	10.1586/17446651.1.5.601
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Article ; Online: Minireview: Molecular targets for obesity therapy in the brain.

Obici, Silvana

Endocrinology

2009 Volume 150, Issue 6, Page(s) 2512–2517

Abstract: Energy balance (intake and expenditure) is under the control of complex and redundant neural pathways that regulate feeding behavior and energy metabolism in response to availability of nutrients in the circulation or in fat stores. A number of hormones ... ...

Abstract	Energy balance (intake and expenditure) is under the control of complex and redundant neural pathways that regulate feeding behavior and energy metabolism in response to availability of nutrients in the circulation or in fat stores. A number of hormones are secreted from peripheral organs and act in the hypothalamus to influence appetite and energy expenditure. This review will summarize recent progress in the identification of the neural pathways that respond to peripheral signals of energy availability such as leptin and macronutrients. Although the impact of environmental factors on obesity is underscored by the modern obesity epidemic, new insights into the pathophysiology of weight control provide new targets for therapeutic intervention for obesity.
MeSH term(s)	Animals ; Body Weight/physiology ; Brain/physiology ; Energy Metabolism/physiology ; Humans ; Hypothalamus/physiology ; Leptin/physiology ; Obesity/physiopathology
Chemical Substances	Leptin
Language	English
Publishing date	2009-06
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2009-0409
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Article ; Online: Brown fat fuel use and regulation of energy homeostasis.

Loyd, Christine / Obici, Silvana

Current opinion in clinical nutrition and metabolic care

2014 Volume 17, Issue 4, Page(s) 368–372

Abstract: Purpose of review: New evidence has recently supported the notion that brown adipose tissue (BAT) is present in adult humans and can play a prominent role in the regulation of body weight and metabolism. This has renewed the efforts to understand the ... ...

Abstract	Purpose of review: New evidence has recently supported the notion that brown adipose tissue (BAT) is present in adult humans and can play a prominent role in the regulation of body weight and metabolism. This has renewed the efforts to understand the physiologic mechanisms by which BAT is activated, which in turn could provide new therapeutic strategies for obesity and diabetes. Recent findings: BAT mass and activity are positively correlated with measures of metabolic health in rodents and humans; however, the amount of functional BAT in adult humans is highly variable with less found in overweight and obese individuals. The impact of BAT in the uptake and utilization of circulating nutrients is systemic, with major effects on whole-body insulin sensitivity and glucose tolerance as illustrated by BAT transplantation in rodents. Furthermore, a host of physiologic conditions and novel peptides/hormones have been implicated in the activation of BAT thermogenesis and/or 'browning' of white adipocytes. Summary: These new findings open the way for novel strategies aimed at increasing BAT mass and activity in obese humans as an important clinical goal in the midst of unprecedented high prevalence of obesity and associated metabolic disorders.
MeSH term(s)	Adipocytes/metabolism ; Adipose Tissue, Brown/metabolism ; Body Weight ; Energy Metabolism/physiology ; Homeostasis/physiology ; Humans ; Insulin Resistance ; Obesity/therapy ; Overweight/therapy ; Thermogenesis/physiology
Language	English
Publishing date	2014-07
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	1460178-3
ISSN	1473-6519 ; 1363-1950
ISSN (online)	1473-6519
ISSN	1363-1950
DOI	10.1097/MCO.0000000000000063
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Article ; Online: Impact of bariatric surgery on the development of diabetic microvascular and macrovascular complications.

Goldberg, Iliya / Nie, Lizhou / Yang, Jie / Docimo, Salvatore / Obici, Silvana / Talamini, Mark / Pryor, Aurora / Spaniolas, Konstantinos

Surgical endoscopy

2020 Volume 35, Issue 7, Page(s) 3923–3931

Abstract: Background: While bariatric surgery has been shown to improve type 2 diabetes (DM) control in the obese population, the effect on long-term DM complications has been less thoroughly investigated. The purpose of this study was to assess the development ... ...

Abstract	Background: While bariatric surgery has been shown to improve type 2 diabetes (DM) control in the obese population, the effect on long-term DM complications has been less thoroughly investigated. The purpose of this study was to assess the development of microvascular and macrovascular complications in obese DM patients undergoing bariatric surgery. Methods: New York patients' records from the SPARCS database in years 2006-2012 were used to identify obese patients with DM. Patients undergoing bariatric surgery were compared with patients managed medically, matched for age and gender. Patients were grouped based on baseline presence of controlled or uncontrolled DM and followed over time for the development of micro- and macrovascular complications. Cumulative incidence of complications was estimated with death treated as a competing risk event. Multivariable proportional sub-distribution hazards models were used to compare the risk of complications among different patient groups after adjusting for possible confounding factors. Results: A total of 88,981 patients were reviewed, including 15,585 (18%) that were treated with bariatric surgery. Surgery patients had significantly lower risk of microvascular complications compared to non-surgery patients (controlled diabetes: HR = 0.40, 95% CI 0.37-0.42; uncontrolled diabetes: HR = 0.51, 95% CI 0.37-0.71). Similarly, the surgical patients were noted to have a significantly lower risk for macrovascular complications compared to non-surgery patients (controlled diabetes: HR = 0.43, 95% CI 0.40-0.46; uncontrolled diabetes: HR = 0.44, 95% CI 0.28-0.69). Cumulative incidence of microvascular complications was lower at 1, 5 and 9 years for the surgical groups for controlled and uncontrolled DM. Similar trends were observed for the macrovascular complications. Conclusions: Bariatric surgery appears to prevent complications of DM. Bariatric surgery patients with DM experienced significantly lower rates of microvascular and macrovascular complications, compared to non-surgically treated comparison group. Bariatric surgery was noted to offer protective benefits for both complicated and non-complicated DM patients. This reduced rate of complications was sustained in the long term.
MeSH term(s)	Bariatric Surgery/adverse effects ; Diabetes Mellitus, Type 2/complications ; Diabetes Mellitus, Type 2/epidemiology ; Humans ; Incidence ; New York ; Obesity/complications ; Obesity/epidemiology
Language	English
Publishing date	2020-08-03
Publishing country	Germany
Document type	Journal Article
ZDB-ID	639039-0
ISSN	1432-2218 ; 0930-2794
ISSN (online)	1432-2218
ISSN	0930-2794
DOI	10.1007/s00464-020-07848-2
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Article ; Online: Oea Signaling Pathways and the Metabolic Benefits of Vertical Sleeve Gastrectomy.

Hutch, Chelsea R / Trakimas, Danielle R / Roelofs, Karen / Pressler, Joshua / Sorrell, Joyce / Cota, Daniela / Obici, Silvana / Sandoval, Darleen A

Annals of surgery

2019 Volume 271, Issue 3, Page(s) 509–518

Abstract: Objective: The aim of this study was to determine whether downstream [peroxisome proliferator-activated-receptor alpha (PPARα) and the G-protein coupled receptor, GPR119] and upstream (a fatty acid translocase, CD36) signaling targets of N- ... ...

Abstract	Objective: The aim of this study was to determine whether downstream [peroxisome proliferator-activated-receptor alpha (PPARα) and the G-protein coupled receptor, GPR119] and upstream (a fatty acid translocase, CD36) signaling targets of N-oleoylethanolamide (OEA) were necessary for weight loss, metabolic improvements, and diet preference following vertical sleeve gastrectomy (VSG). Summary background data: OEA is an anorectic N-acylethanolamine produced from dietary fats within the intestinal lumen that can modulate lipid metabolism, insulin secretion, and energy expenditure by activating targets such as PPARα and GPR119. Methods: Diet-induced obese mice, including wild-type or whole body knockout (KO) of PPARα, GPR119, and CD36, were stratified to either VSG or sham surgery before body weight, body composition, diet preference, and glucose and lipid metabolic endpoints were assessed. Results: We found increased duodenal production of OEA and expression of both GPR119 and CD36 were upregulated in wild-type mice after VSG. However, weight loss and glucose tolerance were improved in response to VSG in PPARαKO, GPR119KO, and CD36KO mice. In fact, VSG corrected hepatic triglyceride dysregulation in CD36KO mice, and circulating triglyceride and cholesterol levels in PPARαKO mice. Lastly, we found PPARα-mediated signaling contributes to macronutrient preference independent of VSG, while removal of CD36 signaling blunts the VSG-induced shift toward carbohydrate preference. Conclusions: In the search for more effective and less invasive therapies to help reverse the global acceleration of obesity and obesity-related disease OEA is a promising candidate; however, our data indicate that it is not an underlying mechanism of the effectiveness of VSG.
MeSH term(s)	Animals ; Disease Models, Animal ; Endocannabinoids/metabolism ; Ethanolamines/metabolism ; Gastrectomy/methods ; Gene Expression ; Glucose Tolerance Test ; Lipids/blood ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Obesity/metabolism ; Obesity/surgery ; Oleic Acids/metabolism ; PPAR alpha/metabolism ; Rats ; Receptors, G-Protein-Coupled/metabolism ; Scavenger Receptors, Class B/metabolism ; Signal Transduction ; Up-Regulation
Chemical Substances	Endocannabinoids ; Ethanolamines ; Gpr119 protein, mouse ; Lipids ; Oleic Acids ; PPAR alpha ; Receptors, G-Protein-Coupled ; Scarb1 protein, mouse ; Scavenger Receptors, Class B ; N-oleoylethanolamine (111-58-0)
Language	English
Publishing date	2019-02-15
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	340-2
ISSN	1528-1140 ; 0003-4932
ISSN (online)	1528-1140
ISSN	0003-4932
DOI	10.1097/SLA.0000000000003093
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Article: Minireview: the brain as a molecular target for diabetic therapy.

Prodi, Elena / Obici, Silvana

Endocrinology

2006 Volume 147, Issue 6, Page(s) 2664–2669

Abstract: Recent evidence highlights the important role of the brain in the control of glucose homeostasis. Hypothalamic centers sense the availability of peripheral nutrients via redundant and overlapping nutrient-induced peripheral signals such as leptin and ... ...

Abstract	Recent evidence highlights the important role of the brain in the control of glucose homeostasis. Hypothalamic centers sense the availability of peripheral nutrients via redundant and overlapping nutrient-induced peripheral signals such as leptin and insulin and via direct metabolic signaling. Responding to nutrient availability, these hypothalamic regions in turn exert a negative feedback not only on food intake but also on endogenous glucose production. Disruptions in the mechanisms of central nervous system nutrient sensing alter these homeostatic responses and contribute to the pathophysiology of obesity and type 2 diabetes. In this review, we discuss the neural and molecular pathways so far identified as possible targets for therapeutic intervention.
MeSH term(s)	Animals ; Brain/drug effects ; Brain/physiology ; Diabetes Mellitus/drug therapy ; Diabetes Mellitus/etiology ; Glucose/metabolism ; Homeostasis ; Humans ; Hypothalamus/physiology ; Insulin/pharmacology ; Leptin/physiology
Chemical Substances	Insulin ; Leptin ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2006-06
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	427856-2
ISSN	1945-7170 ; 0013-7227
ISSN (online)	1945-7170
ISSN	0013-7227
DOI	10.1210/en.2006-0143
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Article: Central nervous system and control of endogenous glucose production.

Demuro, Giovanna / Obici, Silvana

Current diabetes reports

2006 Volume 6, Issue 3, Page(s) 188–193

Abstract: Recent evidence points to the crucial role of the central nervous system in controlling glucose homeostasis. Hypothalamic centers involved in the regulation of energy balance and endogenous glucose production constantly sense fuel availability by ... ...

Abstract	Recent evidence points to the crucial role of the central nervous system in controlling glucose homeostasis. Hypothalamic centers involved in the regulation of energy balance and endogenous glucose production constantly sense fuel availability by receiving and integrating inputs from circulating nutrients and hormones such as insulin and leptin. In response to these peripheral signals, the hypothalamus sends out efferent impulses that restrain food intake and endogenous glucose production. This promotes energy homeostasis and keeps blood glucose levels in the normal range. Disruption of this intricate neural control is likely to occur in type 2 diabetes and obesity and may contribute to defects of glucose homeostasis and insulin resistance common to both diseases. This review summarizes the latest findings on the hypothalamic control of endogenous glucose production, and focuses on the central effects of circulating macronutrients and nutrient-induced hormones.
MeSH term(s)	Fatty Acids/chemistry ; Fatty Acids/metabolism ; Glucose/biosynthesis ; Homeostasis/physiology ; Humans ; Hypothalamus/metabolism ; Insulin/metabolism ; Leptin/metabolism
Chemical Substances	Fatty Acids ; Insulin ; Leptin ; Glucose (IY9XDZ35W2)
Language	English
Publishing date	2006-08-04
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	2065167-3
ISSN	1534-4827
ISSN	1534-4827
DOI	10.1007/s11892-006-0033-8
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Article ; Online: Central nervous system delivery of the antipsychotic olanzapine induces hepatic insulin resistance.

Martins, Paulo J F / Haas, Michael / Obici, Silvana

Diabetes

2010 Volume 59, Issue 10, Page(s) 2418–2425

Abstract: Objective: Olanzapine (OLZ) is an atypical antipsychotic whose clinical efficacy is hampered by side effects including weight gain and diabetes. Recent evidence shows that OLZ alters insulin sensitivity independent of changes in body weight and ... ...

Abstract	Objective: Olanzapine (OLZ) is an atypical antipsychotic whose clinical efficacy is hampered by side effects including weight gain and diabetes. Recent evidence shows that OLZ alters insulin sensitivity independent of changes in body weight and composition. The present study addresses whether OLZ-induced insulin resistance is driven by its central actions. Research design and methods: Sprague-Dawley rats received an intravenous (OLZ-IV group) or intracerebroventricular (OLZ-ICV group) infusion of OLZ or vehicle. Glucose kinetics were assessed before (basal period) and during euglycemic-hyperinsulinemic clamp studies. Results: OLZ-IV caused a transient increase in glycemia and a higher rate of glucose appearance (R(a)) in the basal period. During the hyperinsulinemic clamp, the glucose infusion rate (GIR) required to maintain euglycemia and the rate of glucose utilization (R(d)) were decreased in OLZ-IV, whereas endogenous glucose production (EGP) rate was increased compared with vehicle-IV. Consistent with an elevation in EGP, the OLZ-IV group had higher hepatic mRNA levels for the enzymes glucose-6-phosphatase and phosphoenolpyruvate carboxykinase. Phosphorylation of hypothalamic AMP-activated protein kinase (AMPK) was increased in OLZ-IV rats compared with controls. Similarly, an intracerebroventricular infusion of OLZ resulted in a transient increase in glycemia as well as a higher R(a) in the basal period. During the hyperinsulinemic period, OLZ-ICV caused a decreased GIR, an increased EGP, but no change in R(d). Furthermore, OLZ-ICV rats had increased hepatic gluconeogenic enzymes and elevated hypothalamic neuropeptide-Y and agouti-related protein mRNA levels. Conclusions: Acute central nervous system exposure to OLZ induces hypothalamic AMPK and hepatic insulin resistance, pointing to a hypothalamic site of action for the metabolic dysregulation of atypical antipsychotics.
MeSH term(s)	Animals ; Antipsychotic Agents/administration & dosage ; Antipsychotic Agents/pharmacology ; Benzodiazepines/administration & dosage ; Benzodiazepines/pharmacology ; Blood Glucose/drug effects ; Blood Glucose/metabolism ; Carotid Arteries/physiopathology ; DNA Primers ; Glucose Clamp Technique ; Glucose-6-Phosphatase/drug effects ; Glucose-6-Phosphatase/genetics ; Hyperinsulinism/physiopathology ; Infusions, Intravenous ; Injections, Intraventricular ; Insulin Resistance/physiology ; Intracellular Signaling Peptides and Proteins/drug effects ; Intracellular Signaling Peptides and Proteins/genetics ; Jugular Veins/physiopathology ; Kinetics ; Liver/drug effects ; Liver/physiology ; Male ; Neuropeptides/drug effects ; Neuropeptides/genetics ; Olanzapine ; Orexins ; Pro-Opiomelanocortin/drug effects ; Pro-Opiomelanocortin/genetics ; Rats ; Rats, Sprague-Dawley ; Tubulin/drug effects ; Tubulin/genetics
Chemical Substances	Antipsychotic Agents ; Blood Glucose ; DNA Primers ; Intracellular Signaling Peptides and Proteins ; Neuropeptides ; Orexins ; Tubulin ; Benzodiazepines (12794-10-4) ; Pro-Opiomelanocortin (66796-54-1) ; Glucose-6-Phosphatase (EC 3.1.3.9) ; Olanzapine (N7U69T4SZR)
Language	English
Publishing date	2010-08-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	80085-5
ISSN	1939-327X ; 0012-1797
ISSN (online)	1939-327X
ISSN	0012-1797
DOI	10.2337/db10-0449
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