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Increases in rat adipose blood flows following bolus intraperitoneal injection of glucose (1156.2)
Author(s) -
Yang Hsiaotung,
Rector Scott,
Thorne Pamela,
Chen Xinyue,
Laughlin Harold
Publication year - 2014
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.28.1_supplement.1156.2
Subject(s) - adipose tissue , medicine , endocrinology , bolus (digestion) , kidney , spleen , blood pressure , blood flow , chemistry , intraperitoneal injection
The purpose of this study was to determine the magnitude of increased blood flow (BF) to rat adipose tissue depots that is signaled by hyperglycemia. BF was measured in adult SD rats (422±2.6 g, n=6) after 5 hr fasting with stable isotope labeled microshereres. > 4 hr recovery from arterial catheterizing surgery, BF was determined in conscious rats confined to cage activity at before and 15 min after bolus dextrose (2 g/kg b.w.) intraperitoneal injection (i.p.). Blood glucose level was increased from 144±10.1 to 463±36.3 mg/dl (p<0.001). Arterial blood pressure (BP) (141±5.8 mm Hg), and heart rate (460±10.0 bpm) remained unchanged by hyperglycemia. BFs (ml/min/100 g) in adipose tissues prior to glucose i.p. were as follows: epididymal (22±2.4), retroperitoneal (200±36.4), omental (47±5.4), subcutaneous (38±2.9), and brown fat (369±66.7). Fifteen min post i.p. glucose, BFs showed 11.3, 5.3, 13.1, 3.8, and 1.4 fold increase in those adipose tissues respectively (p<0.01). In addition, hyperglycemia also induced 4‐6 fold increases in BFs in the hind limb muscles, spleen, kidney, and duodenum (p<0.01), BF to the liver was 13.0 fold higher (p<0.001) in the post compared to prior glucose i.p. (22±2.6 ml/min/100 g). The independent effects of insulin were not assessed, but could have contributed to observed changes in BF. These results demonstrate the dramatic effects of 3.2 fold elevated circulating glucose on increases in BFs in adipose, skeletal muscle, and some visceral organs. Supported by NIH HL 36088 (MHL) , VA‐CDA2 (1299‐02) (RSR), and CVM Research Grant of MU (MHL and HTY) Grant Funding Source : NIH HL 36088 (MHL), VA‐CDA2 (1299‐02) (RSR), and CVM Research Grant of MU (MHL and HTY)

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