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Cited by 169Regulation of Appetite and ObesityPancreatic function and diabetesAdipokines, Inflammation, and Metabolic Diseases

Leptin Activates a Novel CNS Mechanism for Insulin-Independent Normalization of Severe Diabetic Hyperglycemia

Open access
German, Jonathan P., Thaler, Joshua P., Wisse, Brent E., Oh-I, Shinsuke, Sarruf, David A., Matsen, Miles E., Fischer, Jonathan D., Taborsky, Gerald J. +2 more·2011·Endocrinology
DOI 10.1210/en.2010-0890PMC PMC3037161
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Abstract

The brain has emerged as a target for the insulin-sensitizing effects of several hormonal and nutrient-related signals. The current studies were undertaken to investigate mechanisms whereby leptin lowers circulating blood glucose levels independently of insulin. After extending previous evidence that leptin infusion directly into the lateral cerebral ventricle ameliorates hyperglycemia in rats with streptozotocin-induced uncontrolled diabetes mellitus, we showed that the underlying mechanism is independent of changes of food intake, urinary glucose excretion, or recovery of pancreatic β-cells. Instead, leptin action in the brain potently suppresses hepatic glucose production while increasing tissue glucose uptake despite persistent, severe insulin deficiency. This leptin action is distinct from its previously reported effect to increase insulin sensitivity in the liver and offers compelling evidence that the brain has the capacity to normalize diabetic hyperglycemia in the presence of sufficient amounts of central nervous system leptin.

AI snapshot

Written from the paper’s full text.

TL;DR

In streptozotocin-induced uncontrolled diabetic rats, intracerebroventricular leptin normalized blood glucose by day 7 independently of food intake, urinary glucose loss, or pancreatic β-cell recovery. The effect involved insulin-independent suppression of hepatic glucose production and increased tissue glucose uptake, with normalization of plasma glucagon and corticosterone.

Key findings

  • Intracerebroventricular leptin (1 g/d) normalized blood glucose by day 7 in STZ-diabetic rats, whereas subcutaneous leptin at the same dose did not; pair feeding to leptin-treated intake also did not attenuate hyperglycemia.
  • Urinary glucose was undetectable in icv leptin-treated diabetic rats versus marked glycosuria in STZ-veh rats; plasma insulin remained very low, pancreatic preproinsulin mRNA was reduced by >95%, and glucose tolerance was near normal despite no increase in circulating insulin.
  • Tracer studies showed icv leptin reduced glucose appearance/HGP to nondiabetic values and increased glucose uptake in red gastrocnemius muscle, brain, BAT, and heart; during a hyperglycemic clamp at approximately 210 mg/dl, HGP was suppressed and glucose utilization increased despite severe insulin deficiency.
  • Hepatic G6Pase and Pepck expression was reduced by icv leptin; plasma glucagon and corticosterone elevations in STZ diabetes were prevented by icv leptin; hepatic Igfbp2 mRNA was increased >25-fold in diabetic rats and further increased by leptin, which the authors argue is unlikely to explain the HGP effect.

Methods

  • Adult male Wistar rats received two daily sc injections of STZ (40 mg/kg body weight) to induce uncontrolled diabetes, plus lateral ventricle cannula and sc osmotic minipump for icv vehicle or leptin (1 g/d) for up to 11 days; five groups (n = 7–9 per group): veh-veh, STZ-veh, STZ-leptin, STZ-veh-pair-fed, and STZ-leptin-sc.
  • Daily food intake, body weight, water intake, and blood glucose were measured; ip glucose tolerance tests (2 g/kg) were performed on day 9; arterial catheters were used for plasma glucagon, corticosterone, and catecholamine measurements.
  • Glucose turnover was assessed with [3-3H]glucose and 2[14C]deoxyglucose tracer dilution, including a hyperglycemic clamp at approximately 210 mg/dl; hepatic gene expression was measured by real-time PCR, and liver triglyceride/glycogen and body composition were also analyzed.

Limitations

  • The paper states that Rd could not be compared between icv leptin-treated and veh-treated STZ-diabetic rats because glycosuria confounds Rd; it also states that whether reduced glucagon contributes to, or results from, leptin-mediated resolution of hyperglycemia is unknown, and that mechanisms of leptin regulation of the hypothalamic-pituitary-adrenal axis remain incompletely understood.
  • The paper states that autonomic/SNS involvement is suspected but not directly tested here; it notes that prior denervation or adrenergic blockade studies did not measure Rg.
  • Evident from the text: findings are limited to male Wistar rats with STZ-induced diabetes and short-term central leptin infusion, so human type 1 diabetes and long-term outcomes are not established; causal roles of glucagon and corticosterone normalization are not definitively separated from other mechanisms.

Model-written summary. Check it against the paper before relying on it.

Integrity signals

Registry

Crossref · 10.1210/en.2010-0890

Cites

57 of 57 references verified0 citation errors · 0 not checkable

Statistics

Nothing to recompute.

Claims the paper makes

0 of 60 cited sources checked · 0 supported · 0 flagged

  • Findingown data

    CNS leptin normalizes elevated plasma corticosterone levels in STZ-diabetic rats.

    “Plasma corticosterone levels were similarly elevated in animals with STZ diabetes, a response also prevented by icv leptin but not PF (Fig. 6B).”
    Quote in the paperSubstantial claim
  • Findingown data
    § Leptin Activates a Novel CNS Mechanism for Insulin-Independent Normalization of Severe Diabetic Hyperglycemia

    CNS leptin normalizes elevated plasma glucagon levels in STZ-diabetic rats.

    “Although the action of leptin in the CNS was also associated with normalization of elevated plasma glucagon levels, consistent with an earlier report (4), our data suggest that factors, in addition to glucagon, contribute to the glucoselowering effect of CNS leptin action.”
    • Also stated in: § CNS leptin infusion normalizes plasma glucagon and corticosterone levels in STZ-induced diabetes · plain
      “the elevation in plasma glucagon levels observed in STZ-treated animals was prevented by central leptin administration (Fig. 6A).”
    Quote in the paperNot a substantial claim
  • Findingown data
    § Leptin Activates a Novel CNS Mechanism for Insulin-Independent Normalization of Severe Diabetic Hyperglycemia

    CNS leptin administration increases tissue glucose uptake (Rg) in STZ-diabetic rats.

    “leptin action in the brain potently suppresses hepatic glucose production while increasing tissue glucose uptake despite persistent, severe insulin deficiency.”
    • Also stated in: § Effect of icv leptin infusion on HGP and glucose uptake in STZ-induced diabetes · plain
      “glucose uptake was significantly increased in red gastrocnemius muscle and brain in STZdiabetic animals that received icv leptin relative to veh (Fig. 3C).”
    • Also stated in: § Discussion · boosted
      “we demonstrate that leptin acts in the CNS to potently inhibit glucose production and simultaneously increase tissue glucose utilization in diabetic animals.”
    Quote in the paperSubstantial claim
  • Findingown data
    § Leptin Activates a Novel CNS Mechanism for Insulin-Independent Normalization of Severe Diabetic Hyperglycemia

    The glucose-lowering effect of CNS leptin in STZ-diabetic rats is not due to reduced food intake.

    “we showed that the underlying mechanism is independent of changes of food intake, urinary glucose excretion, or recovery of pancreatic ␤-cells.”
    • Also stated in: § CNS leptin infusion normalizes blood glucose levels in STZ-induced diabetes · plain
      “This effect was due neither to a leptin-mediated reversal of diabetic hyperphagia, because hyperglycemia was not attenuated in STZ-veh-PF animals”
    • Also stated in: § Discussion · plain
      “via a mechanism that cannot be explained by reduced food intake, increased urinary glucose losses, or recovery of pancreatic ␤-cells”
    Quote in the paperSubstantial claim
  • Findingown data
    § Leptin Activates a Novel CNS Mechanism for Insulin-Independent Normalization of Severe Diabetic Hyperglycemia

    CNS leptin administration suppresses hepatic glucose production (HGP) in STZ-diabetic rats.

    “leptin action in the brain potently suppresses hepatic glucose production while increasing tissue glucose uptake despite persistent, severe insulin deficiency.”
    • Also stated in: § Effect of icv leptin infusion on HGP and glucose uptake in STZ-induced diabetes · hedged
      “Central leptin administration dramatically reduced Ra to nondiabetic control values (Fig. 3A), strongly suggesting that normalization of diabetic hyperglycemia resulted, at least in part, from reduced HGP.”
    • Also stated in: § Discussion · boosted
      “we demonstrate that leptin acts in the CNS to potently inhibit glucose production and simultaneously increase tissue glucose utilization in diabetic animals.”
    Quote in the paperSubstantial claim
  • May combine two claims. 16
  • Classified as probably not a substantial claim. 4

  • May combine two claims.

    Findingown data

    Plasma NEFAs and ketone bodies are elevated in STZ-veh animals and normalized with icv leptin administration but only after blood glucose levels had returned to normal.

    “plasma levels of NEFAs and ketone bodies were also elevated in STZ-veh animals and normalized with icv leptin administration but only after blood glucose levels had returned to normal (Fig. 6, E and F).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    Water intake is markedly increased in both groups of STZ-veh-treated animals, whereas water intake in diabetic animals receiving icv leptin is equivalent to that of nondiabetic controls.

    “water intake was markedly increased in both groups of STZ-veh-treated animals, owing to the dehydrating effect of pronounced glycosuria in uDM (26), whereas water intake in diabetic animals receiving icv leptin was equivalent to that of nondiabetic controls (Fig. 2B).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Leptin-treated STZ-diabetic rats exhibit similar weight loss to STZ-diabetic rats receiving icv veh but greater loss of fat mass.

    “leptin-treated STZ-diabetic rats exhibited similar weight loss to STZ-diabetic rats receiving icv veh but exhibited a greater loss of fat mass (Supplemental Fig. 1”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingown data

    In nondiabetic animals, plasma insulin and C-peptide levels are significantly increased during hyperglycemic clamp, resulting in complete suppression of HGP and enhancement of glucose utilization by more than 250%.

    “In nondiabetic animals, plasma insulin and C-peptide levels were significantly increased during the hyperglycemic clamp (P Ͻ 0.05) (Fig. 5, A and B), resulting in complete suppression of HGP and enhancement of glucose utilization by more than 250% (Fig. 5, E-H).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    During hyperglycemic clamp, HGP is suppressed and glucose utilization is increased in STZ-diabetic rats receiving icv leptin despite persistent severe insulin deficiency.

    “Similarly, despite persistent, severe insulin deficiency, HGP was suppressed and glucose utilization was increased in STZ-diabetic rats receiving icv leptin, although less than that observed in nondiabetic animals (Fig. 5, E-H).”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    Food intake is significantly increased by d 5 after STZ administration in diabetic animals receiving icv veh, and this effect is completely blocked by icv leptin.

    “food intake was significantly increased by d 5 after STZ administration in diabetic animals receiving icv veh, and this effect was completely blocked by icv leptin (Fig. 1C).”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Findingcitation

    Physiological leptin replacement is sufficient to normalize plasma glucagon levels but has little effect on diabetic hyperglycemia in rats with STZ diabetes.

    “We recently observed that in rats with STZ diabetes, physiological leptin replacement is sufficient to normalize plasma glucagon levels but has little effect on diabetic hyperglycemia (20).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [20] German, 2010, Leptin deficiency causes insulin resistance induced by uncontrolled diabetes., Diabetes source

      Not checked in the free run.

  • May combine two claims.

    Findingown data

    CNS leptin suppresses HGP and increases glucose utilization in uDM during a hyperglycemic clamp.

    “CNS leptin suppresses HGP and increases glucose utilization in uDM during a hyperglycemic clamp.”
    Quote in the paperSubstantial claim

  • May combine two claims.

    Findingown data

    CNS leptin normalizes plasma glucagon and corticosterone levels in uDM.

    “CNS leptin normalizes plasma glucagon and corticosterone levels in uDM.”
    Quote in the paperSubstantial claim

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation
    § Leptin Activates a Novel CNS Mechanism for Insulin-Independent Normalization of Severe Diabetic Hyperglycemia

    Accumulating evidence suggests that leptin, insulin, and nutrient-related signals in the CNS improve hepatic insulin sensitivity.

    “Although accumulating evidence suggests that leptin (10 -13), insulin (14,15), and nutrient-related signals (16 -18) in the CNS improve hepatic insulin sensitivity”
    Quote in the paperNot a substantial claim0 of 9 sources checked
    • cites [10] Liu, 1998, Intracerebroventricular leptin regulates hepatic but not peripheral glucose fluxes., J Biol Chem source

      Not checked in the free run.

    • cites [11] Pocai, 2005, Central leptin acutely reverses diet-induced hepatic insulin resistance., Diabetes source

      Not checked in the free run.

    • cites [12] Park, 2008, Long-term effects of central leptin and resistin on body weight, insulin resistance, and β-cell function and mass by the modulation of hypothalamic leptin and insulin signaling., Endocrinology source

      Not checked in the free run.

    • cites [13] German, 2009, Hypothalamic leptin signaling regulates hepatic insulin sensitivity via a neurocircuit involving the vagus nerve., Endocrinology source

      Not checked in the free run.

    • cites [14] Obici, 2002, Hypothalamic insulin signaling is required for inhibition of glucose production., Nat Med source

      Not checked in the free run.

    • cites [15] Pocai, 2005, Hypothalamic K(ATP) channels control hepatic glucose production., Nature source

      Not checked in the free run.

    • cites [16] Obici, 2002, Central administration of oleic acid inhibits glucose production and food intake., Diabetes source

      Not checked in the free run.

    • cites [17] Lam, 2005, Hypothalamic sensing of circulating fatty acids is required for glucose homeostasis., Nat Med source

      Not checked in the free run.

    • cites [18] Pocai, 2005, A brain-liver circuit regulates glucose homeostasis., Cell Metabolism source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    Insulin action in the brain of nondiabetic animals lowers ambient glycemia by increasing hepatic insulin sensitivity.

    “Several lines of evidence suggest that like leptin, insulin action in the brain of nondiabetic animals lowers ambient glycemia by increasing hepatic insulin sensitivity (14,15).”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [14] Obici, 2002, Hypothalamic insulin signaling is required for inhibition of glucose production., Nat Med source

      Not checked in the free run.

    • cites [15] Pocai, 2005, Hypothalamic K(ATP) channels control hepatic glucose production., Nature source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation
    § Leptin Activates a Novel CNS Mechanism for Insulin-Independent Normalization of Severe Diabetic Hyperglycemia

    Leptin administration directly into the brain normalizes blood glucose in rats with uDM at doses that are ineffective when administered peripherally.

    “leptin adminis-tration directly into the brain normalizes blood glucose in rats with uDM (5)(6)(7)(8)(9) at doses that are ineffective when administered peripherally.”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites 5)(6)(7)(8)(9

      Not checked in the free run.

  • May combine two claims.

    Interpretationreasoning

    Icv leptin treatment reduces food intake and stimulates energy expenditure.

    “These data suggest that icv leptin treatment reduces food intake and stimulates energy expenditure”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    Physiological leptin replacement is sufficient to normalize circulating glucagon and corticosterone levels, yet does not reverse hyperglycemia in rats with STZ diabetes.

    “we recently reported that in rats with STZ diabetes, physiological leptin replacement is sufficient to normalize cir-culating glucagon and corticosterone levels, yet does not reverse hyperglycemia (20).”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [20] German, 2010, Leptin deficiency causes insulin resistance induced by uncontrolled diabetes., Diabetes source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Hepatic Igfbp-2 expression is tonically inhibited by insulin and dramatically up-regulated by insulin deficiency.

    “hepatic Igfbp-2 expression is tonically inhibited by insulin and hence dramatically up-regulated by insulin deficiency (50 -52).”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [50] Böni-Schnetzler, 1990, Insulin regulates the expression of the insulin-like growth factor binding protein 2 mRNA in rat hepatocytes., Mol Endocrinol source

      Not checked in the free run.

    • cites [51] Ooi, 1992, Post-transcriptional regulation of insulin-like growth factor binding protein-2 mRNA in diabetic rat liver., Biochem Biophys Res Commun source

      Not checked in the free run.

    • cites [52] White, 1993, Insulin-like growth-factor binding protein (IGFBP) serum levels and hepatic IGFBP-2 and -3 mRNA expression in diabetic and insulin-treated swine (Sus scrofa)., Comp Biochem Physiol B source

      Not checked in the free run.

  • May combine two claims.

    Premisecitation

    Conditions associated with leptin deficiency, such as fasting and uDM, raise corticosterone levels via a mechanism that can be reversed with leptin treatment.

    “conditions associated with leptin deficiency, such as fasting and uDM, clearly raise corticosterone levels via a mechanism that can be reversed with leptin treatment (44,45,49).”
    Quote in the paperSubstantial claim0 of 3 sources checked
    • cites [44] Schwartz, 1997, Evidence that elevated plasma corticosterone levels are the cause of reduced hypothalamic corticotrophin-releasing hormone gene expression in diabetes., Regul Pept source

      Not checked in the free run.

    • cites [45] Strack, 1995, Glucocorticoids and insulin: reciprocal signals for energy balance., Am J Physiol

      Not checked in the free run.

    • cites [49] Ahima, 1996, Role of leptin in the neuroendocrince response to fasting., Nature source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S3 (load-bearing).

    Premisecitation

    A shared neuronal mechanism mediates effects of both insulin and leptin on glucose metabolism.

    “suggesting a shared neuronal mechanism mediating effects of both hormones on glucose metabolism (34,35).”
    Quote in the paperNot a substantial claim0 of 2 sources checked
    • cites [34] Obici, 2002, Decreasing hypothalamic insulin receptors causes hyperphagia and insulin resistance in rats., Nat Neurosci source

      Not checked in the free run.

    • cites [35] Morton, 2005, Leptin regulates insulin sensitivity via phosphatidylinositol-3-OH kinase signaling in mediobasal hypothalamic neurons., Cell Metab source

      Not checked in the free run.

  • Probably not a substantial claim: may not pass S4 (based).

    Interpretationnone given

    These observations are distinct from any previously described CNS leptin action.

    “These observations are distinct from any previously described CNS leptin action”
    Quote in the paperNot a substantial claim

  • May combine two claims.

    Premisecitation

    Activation of β3-adrenergic receptors is not required or sufficient to mediate the effects of leptin on blood glucose levels.

    “nor was activation of the ␤3-adrenergic receptors required or sufficient to mediate the effects of leptin on blood glucose levels (7)”
    Quote in the paperSubstantial claim0 of 1 sources checked
    • cites [7] da Silva, 2006, Chronic antidiabetic and cardiovascular actions of leptin: role of CNS and increased adrenergic activity., Am J Physiol Regul Integr Comp Physiol source

      Not checked in the free run.

  • May combine two claims.

    Interpretationown data

    icv leptin normalizes blood glucose levels in STZ-diabetic rats at least in part via an insulin-independent mechanism that increases glucose utilization in tissues such as BAT and skeletal muscle.

    “Based on these data, we infer that icv leptin normalizes blood glucose levels in STZ-diabetic rats at least in part via an insulin-independent mechanism that increases glucose utilization in tissues such as BAT and skeletal muscle.”
    Quote in the paperSubstantial claim
20 of 20

  • The authors state this as an assumption.

    How CNS leptin signaling normalizes diabetic hyperglycemia in uDM, and whether this involves leptin-dependent effects on HGP or Rg, is unknown.

    “how CNS leptin signaling normalizes diabetic hyperglycemia in uDM, and whether this involves leptin-dependent effects on hepatic glucose production (HGP) or tissue glucose uptake (Rg), is unknown.”

  • The paper relies on this without support.

    Changes in plasma glucagon do not affect glucose utilization.

    “an effect not readily explained by changes of plasma glucagon (which does not affect glucose utilization)”
2 of 2

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Continuous infusion of leptin directly into the brain normalizes blood glucose levels in STZ-induced diabetic rats via a mechanism that cannot be explained by reduced food intake, increased urinary glucose losses, or recovery of pancreatic β-cells.

    “we recently found that continuous infusion of leptin directly into the brain normalizes blood glucose levels in STZ-induced diabetic rats via a mechanism that cannot be explained by reduced food intake, increased urinary glucose losses or a recovery of pancreatic β-cells.”

    From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [67]

  • This leptin action is distinct from its previously reported effect to increase insulin sensitivity in the liver and offers compelling evidence of a novel mechanism through which the brain normalizes diabetic hyperglycemia without the need for insulin.

    “This leptin action is distinct from its previously reported effect to increase insulin sensitivity in the liver (66, 146), and offers compelling evidence of a novel mechanism through which the brain normalizes diabetic hyperglycemia without the need for insulin (67).”

    From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [67]

  • Leptin action in the brain potently suppresses hepatic glucose production while increasing tissue glucose uptake despite persistent, severe insulin deficiency.

    “Instead, leptin action in the brain potently suppressed hepatic glucose production while increasing tissue glucose uptake despite persistent, severe insulin deficiency (67).”

    From Leptin and the Central Nervous System Control of Glucose Metabolism (2011) · cites this paper as [67]

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

Each contradiction between two passages listed here was confirmed by an independent check.

  • Incorrect figure panel cited for norepinephrine

    Minor

    The text cites Figure 6A for norepinephrine, but the figure caption identifies panel A as glucagon and panel C as norepinephrine.

1 of 1

Cites

Flagged first, then by citations

8 of the 65 references couldn’t be matched to a known paper.

Research works printed but not linked: 1

  1. Maghnie, 2003, Diabetes insipidus., Horm Res, 59, 42

Cited by

Sorted by citations

Related

Authors
German, J. P., Thaler, J. P., Wisse, B. E., Oh-I, S., Sarruf, D. A., Matsen, M. E., Fischer, J. D., Taborsky, G. J., Schwartz, M. W., & Morton, G. J.
Affiliations
  • University of Washington (US)
  • Diabetes and Obesity Center of Excellence (J.P.G., J.P.T., B.E.W., S.O.-I., D.A.S., M.E.M., J.D.F., M.W.S., G.J.M.), Department of Medicine, University of Washington, Seattle, Washington 98109
  • VA Puget Sound Health Care System (US)
Corresponding author
Morton, Gregory J.
ORCID
Venue
Endocrinology
Publisher
The Endocrine Society
Published
2010-12-15
Volume
152
Issue
2
Pages
394-404
ISSN
  • 0013-7227 (ISSN-L)
  • 1945-7170
DOI
10.1210/en.2010-0890
PMC
PMC3037161
OpenAlex
W1996800212
Semantic Scholar
7c46f9454e2b40dacf481b15d5c0a823b6dc64a7
Cited by
169
References
65
Citations by year
2026: 1 · 2025: 8 · 2024: 7 · 2023: 4 · 2022: 7 · 2021: 12 · 2020: 10 · 2019: 10 · 2018: 6 · 2017: 14 · 2016: 18 · 2015: 23 · 2014: 14 · 2013: 16 · 2012: 11
FWCI
4.94
Type
journal article
Language
en
Open access
Locations
  • Endocrinology (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
Funders
  • U.S. Department of Veterans Affairs
  • University of Washington
  • National Institutes of Health (1u24dk076126-01)
  • National Institute of Diabetes and Digestive and Kidney Diseases (R01DK074758, DK-083042, U24-DK076126, DK 035816, DK-050154-13, R56DK050154, R01DK050154, R01DK090320, P30DK035816, R01DK083042)
Topics
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
  • Health Sciences › Medicine › Surgery › Pancreatic function and diabetes
  • Health Sciences › Medicine › Epidemiology › Adipokines, Inflammation, and Metabolic Diseases
Keywords
leptin, diabetic hyperglycemia, insulin-independent glucose regulation, hepatic glucose production, tissue glucose uptake, streptozotocin-induced diabetes, insulin deficiency
MeSH terms
Animals, Blood Glucose, Body Composition, Brain, Corticosterone, Diabetes Mellitus, Experimental, Glucagon, Glucose Tolerance Test, Hyperglycemia, Insulin, Male, Rats, Wistar, Reverse Transcriptase Polymerase Chain Reaction, Leptin, Rats

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