Journal
DIABETES
Volume 52, Issue 3, Pages 663-666Publisher
AMER DIABETES ASSOC
DOI: 10.2337/diabetes.52.3.663
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Funding
- NIDDK NIH HHS [R37 DK 20495, R01 DK 40936, P01 DK 45735, R01 DK040936] Funding Source: Medline
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We have previously reported that a glucosensor integrating hormonal responses to hypoglycemia is located in the ventromedial hypothalamus (VMH) and that local VMH glucose perfusion blocks counterregulatory hormone responses. To determine whether the by-product of glucose metabolism, lactate, can function within the VMH as an alternative for glucose, we delivered lactate locally to the VMH, during systemic hypoglycemia. For this purpose, we combined bilateral VMH microdialysis perfusion (metabolically active L-lactate or its nonmetabolizable D-isomer) with a euglycemic-hypoglycemic clamp in conscious chronically catheterized SpragueDawley rats. Local VMH perfusion with L-lactate decreased counterregulatory hormone responses to hypoglycemia by 80-85% as compared with the nonmetabolizable D-lactate control. Moreover, hormonal suppression with L-lactate was accompanied by an approximate fourfold increase in the amount of exogenous glucose infused to maintain a stable hypoglycemic plateau (P < 0.05). In conclusion, the glucose-sensing mechanism in the VMH responds to lactate and, thus, is not specific for glucose. This implies that the VMH may act as a fuel sensor rather than as a glucose sensor.
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