GTTs and ITTs. A: GTTs of WT (◇), LepTg (♦), Akita (open circles), and LepTg:Akita (closed circles) mice at 8 and 16 weeks of age. GTTs and ITTs. A: GTTs.

Slides:



Advertisements
Similar presentations
Volume 4, Issue 12, Pages (December 2015)
Advertisements

Impaired glucose tolerance in adult S1/3 KO mice on a normal chow
The worldwide association between mean annual temperature and age-adjusted, sex-adjusted, income-adjusted and obesity-adjusted prevalence of raised fasting.
Change in random blood glucose level, body weight, and intraperitoneal glucose tolerance test (IPGTT) in streptozotocin (STZ)-induced diabetic mice. Change.
(A) Body weight (g). (A) Body weight (g). T2DM: n=6 per group. *p
Treatment with AAV8‐hAAT‐FGF21 improves insulin sensitivity and glucose tolerance Treatment with AAV8‐hAAT‐FGF21 improves insulin sensitivity and glucose.
Hyperinsulinemic-euglycemic clamps revealed that obese TPL2KO mice have an improved insulin sensitivity compared with obese WT mice. Hyperinsulinemic-euglycemic.
Response of BW YPO consomic males to glucose and insulin challenges.
Overexpression of BTG2 resulted in an increase in hepatic gluconeogenesis. Overexpression of BTG2 resulted in an increase in hepatic gluconeogenesis. A:
Deletion of neuronal insulin receptor signaling reduces TG secretion, while the targeted knockout of insulin receptors restricted to the periphery increases.
Body weight, blood glucose, and iron status in STZ-induced type 1 diabetic rats with or without insulin therapy. Body weight, blood glucose, and iron status.
Glucose, insulin, and AGE levels during an OGC before and after RT
Exogenous CRP administration causes fasting hyperglycemia and hyperinsulinemia without altering body composition. Exogenous CRP administration causes fasting.
1018-NT-β-cell clusters protect mice from STZ-induced diabetes.
WASH cKO mice display a normal pancreatic development.
TG-CRP mice display fasting hyperglycemia, hyperinsulinemia, and insulin resistance. TG-CRP mice display fasting hyperglycemia, hyperinsulinemia, and insulin.
GSIS. GSIS. In vivo: serum insulin levels at fasting state and 30 min after glucose injection (A) and the fold change in serum insulin after glucose loading.
Glucose infusion rate required to maintain the hyperglycemic clamp during the experimental period in sedentary and exercised dogs receiving basal or elevated.
Activation of β-adrenoceptors improves glucose tolerance in diabetic animals and increases glucose uptake in vivo, ex vivo, and in vitro. Activation of.
A: The change of plasma glucose in opioid μ-receptor knockout diabetic mice and wild-type controls receiving an oral intake of metformin (100 mg/kg). A:
Nrf2−/− mice suffered greater renal damage by STZ compared with Nrf2+/+ mice. Nrf2−/− mice suffered greater renal damage by STZ compared with Nrf2+/+ mice.
Modulation of insulin sensitivity by IL-6 in mice: A lack of PTP1B prevents chronic effects of IL-6. Modulation of insulin sensitivity by IL-6 in mice:
Left columns: Plasma glucose and serum insulin concentrations, circulating TF-PCA, and FVIIa activity before and during 24 h of selective hyperglycemia.
Comparison of women carrying a male fetus and those carrying a female fetus, with respect to mean adjusted blood glucose levels during the OGTT (A), mean.
Loss of protection by linagliptin against obesity-related inflammation and insulin resistance in MIP-1α−/− mice. Loss of protection by linagliptin against.
Glucose tolerance in WT and TRPM2-KO mice.
Transgenic restoration of long-chain n-3 PUFA protects against obesity-linked insulin resistance and glucose intolerance. Transgenic restoration of long-chain.
Immunoblotting samples (A and F) and densitometric analysis of ASC1 (B and G), NLRP3 (C and H), TNFα (D and I) and Caspase-1 (E and J) expression in the.
Effects of in vivo AICAR treatment on blood glucose and lactate concentrations. Effects of in vivo AICAR treatment on blood glucose and lactate concentrations.
At 6 months of age, PPARγ deletion in late osteoblast/osteocyte controls glucose homeostasis by increasing metabolic rate and glucose uptake in WAT, BAT,
ΑGLP-1R−/− mice show glucose intolerance and disturbed glucagon secretion in response to i.p. glucose administration. αGLP-1R−/− mice show glucose intolerance.
Effects of the β-cell–specific expression of mKL on blood glucose levels, glucose tolerance, insulin sensitivity, and plasma insulin levels in STZ-induced.
Somatostatin released by δ-cells exerts a tonic inhibition on glucagon and insulin secretion but is not required for the glucagonostatic effect of glucose.
BAFF-deficient (BAFFnull) and anti-BAFF antibody (Ab)–treated obese mice exhibit superior glucose metabolic control compared with WT and Bnull mice. BAFF-deficient.
Substrate oxidation and contractile performance of Akita hearts
GLP-1 and gastrin combination therapy restores normoglycemia in NOD mice. GLP-1 and gastrin combination therapy restores normoglycemia in NOD mice. Beginning.
A: Chemical structure of pterosin A
GLP-1 and gastrin combination therapy increases pancreatic insulin content (A) and β-cell mass (B) in NOD mice. GLP-1 and gastrin combination therapy increases.
Chop deletion preserves β-cell function in P58IPK−/− mice.
Reduced OXPHOS expression and increased UCP expression.
Adoptive transfer of purified activated G9Cα−/−
USP2–45 regulates hepatic gluconeogenesis.
Atrasentan reduces albuminuria in diabetic apoE KO mice.
Diabetes development in B6.H-2g7/RIP-B7.1 and control mice.
Effect of anandamide on blood glucose clearance and insulin sensitivity. Effect of anandamide on blood glucose clearance and insulin sensitivity. A: Intraperitoneal.
Mean (±SE) plasma glucose concentrations before, during, and after infusions of octreotide (with growth hormone) with saline (•), with insulin replacement.
HFD feeding induced insulin resistance in TRIB3 MOE mice.
High-glucose–induced insulin resistance in TRIB3 MOE mice.
Liver fibrosis after CCl4 injury in 5αR1-KO and WT mice.
Mice fed GP-SPI diet show improved fasting glucose and oral glucose tolerance. Mice fed GP-SPI diet show improved fasting glucose and oral glucose tolerance.
Food intake in response to central infusion of glucose (squares) or insulin (triangles) and in response to successive central infusion of insulin, insulin.
Insulin resistance and hepatic steatosis in ASKO mice.
Treatment of ob/ob mice with TTR-ASOs improves insulin sensitivity.
MϕRIP140KD mice exhibit improved metabolic phenotypes.
Effects of Rosi treatment on ASKO mice.
Effects of chow-diet feeding on control and TRIB3 MOE mice.
Effects of berberine on in vivo metabolism in two animal models of insulin resistance. Effects of berberine on in vivo metabolism in two animal models.
AKT thr308 phosphorylation related to total AKT2 protein in SOL muscle (m. soleus) (A) and EDL muscle (m. extensor digitorum longus) (D) and AKT ser472.
Urinary albumin excretion and histology of glomeruli.
Glucose-stimulated insulin secretion, plasma glucagon levels, and pancreatic hormone contents. Glucose-stimulated insulin secretion, plasma glucagon levels,
Average percent change in serum leptin and soluble leptin receptor (sOB-R) levels in response to rhLeptin administration at a low dose (0.01 mg/kg) (n.
High-fat diet–induced glucose intolerance is prevented in ghrelin knockout (Ghr-KO) mice. High-fat diet–induced glucose intolerance is prevented in ghrelin.
Loss of Phb2 in β-cells induces development of diabetes over a 3-week period in β-Phb2−/− mice. Loss of Phb2 in β-cells induces development of diabetes.
Blood glucose levels in chicken embryos.
Mice lacking Y1 receptor in the hematopoietic compartment remain healthy under normal chow feeding conditions. Mice lacking Y1 receptor in the hematopoietic.
Effects of rhein on FBG (A) and glucose intolerance (B) in db/db mice.
Deficiency of adipocyte IKKβ does not affect diet-induced weigh gain but results in an exaggerated diabetic phenotype when challenged with an HFD. A: IKKβ.
Glycemic control and body weight over 52 weeks.
SORCS1 and SORCS3 control energy balance and orexigenic peptide production A, BBlood glucose (A) and insulin (B) levels after overnight fasting in 9‐month‐old.
Postoperative blood glucose levels and total insulin requirement.
Presentation transcript:

GTTs and ITTs. A: GTTs of WT (◇), LepTg (♦), Akita (open circles), and LepTg:Akita (closed circles) mice at 8 and 16 weeks of age. GTTs and ITTs. A: GTTs of WT (◇), LepTg (♦), Akita (open circles), and LepTg:Akita (closed circles) mice at 8 and 16 weeks of age. Blood glucose levels are shown at indicated times after glucose injections (1 g/kg body wt i.p.; n ≥4 in each group). B: ITTs of WT (◇), LepTg (♦), Akita (○), and LepTg:Akita (●) mice at 8, 18, and 28 weeks of age. Percent changes in blood glucose levels are shown at indicated times after injection of insulin (0.5 units/kg body wt i.p.; n ≥ 4 in each group). Dashed line indicates detection limit of 600 mg/dL. Data are expressed as means ± SE. §P < 0.05, §§P < 0.01 for WT vs. Akita, ‡P < 0.05, ‡‡P < 0.01 for WT vs. LepTg:Akita, ★P < 0.05, ★★P < 0.01 for LepTg vs. LepTg:Akita, *P < 0.05, and **P < 0.01 for Akita vs. LepTg:Akita. Masaki Naito et al. Diabetes 2011;60:2265-2273 ©2011 by American Diabetes Association