Feeding metabolic response

Basal metabolic rate is decreased under conditions of starvation (including dieting as noted above one more reason why it is tough to lose weight) and increased under conditions of feeding. These responses tend to keep body weight constant. Thyroid hormone increases basal metabolic rate. Hyperthyroid people tend to be slender. 

Black, D. (1983). The metabolic response to starvation and re-feeding in fish. Ph.D. thesis, University of Aberdeen, Scotland. 

Wang, T, D.L. Hartzell, B.S. Rose,W.P. Flatt, M.G. Hulsey, N.K. Menon, R.A. Makula and C.A. Baile, 1999. Metabolic responses to intracerebroventricular leptin and restricted feeding. Physiol Behav 65, 839-848. 

The various effects of benzodiazepines given to the mothers on the foetus have been reviewed (39 ). Attention is drawn to foetal hypotonia, reluctance to feed, and impaired metabolic response to cold stress. Estimations of plasma diazepam levels in the newborn have shown that diazepam and its active metabolites were present in foetal blood up to 8 days after delivery. 

For some toxins it is possible to demonstrate an apparent improvement in functional response at levels of exposure which are below a threshold. This effect, which has been termed hormesis , is most effectively demonstrated in the consistently improved longevity of animals whose caloric intake is restricted rather than allowing them to feed ad lib (Tannenbaum, 1942). Clearly in this instance, the observed effects are the result of exposure to a complex mixture of chemicals whose metabolism determines the total amount of energy available to the organism. But it is also possible to show similar effects when single chemicals such as alcohol (Maclure, 1993), or caffeic acid (Lutz et al., 1997) are administered, as well as for more toxic chemicals such as arsenic (Pisciotto and Graziano, 1980) or even tetrachloro-p-dibenzodioxin (TCDD) ( Huff et al., 1994) when administered at very low doses. It is possible that there are toxins that effect a modest, reversible disruption in homeostasis which results in an over-compensation, and that this is the mechanism of the beneficial effect observed. These effects would not be observed in the animal bioassays since to show them it would be necessary to have at least three dose groups below the NOAEL. In addition, the strain of animal used would have to have a very low incidence of disease to show any effect. 

Since the presumed cytosolic pathway interfaces directly with the network of secondary metabolism, the observed induction of DS-Co and CM-2 isozymes in response to wounding was expected. However, the even greater response of plastidic isozymes was unexpected. Perhaps the increased pull on carbohydrate metabolism in the cytosol affects the balance of substrates feeding into the aromatic pathway of the plastid. If so, a tendency to starvation for pathway endproducts may trigger derepression of the plastidic-pathway isozymes. 

There are several known effects of BHA treatment which have been proposed to reduce the levels of reactive metabolites of BP which bind to DNA. It has been demonstrated that BHA feeding alters the microsomal mixed-function oxidase system in mice and rats (7,17-19). Several studies suggest that BHA treatment does not decrease the amounts of BP-7, 8-diol formed (7,20,21) whereas there is some indirect evidence that BHA treatment alters the metabolism of BP-7,8-diol (3,20) An induction by BHA of an lsozyme(s) of cytochrome P-450, which has kinetics of metabolism of BP-7,8-diol different than that of the constitutive isozyme(s), could account for the BHA-induced shifts in the dose-response curve for BPDEI-DNA adduct levels (15). 

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