METABOLIC INTERACTIONS BETWEEN SURPLUS DIETARY ENERGY-INTAKE AND CIGARETTE-SMOKING OR ITS CESSATION

Cigarette smoking (CS) alters lipid metabolism and is associated clini cally with an atherogenic lipid profile. We recently showed that, unde r controlled eucaloric dietary conditions, CS stimulates lipolysis wit hout increasing oxidation of fat and that cessation of CS does not res ult in a rebound tendency to synthesize or store fat. We asked here wh ether the ad libitum intake of surplus dietary energy interacts with t he metabolic effects of CS or its cessation. Eight male heavy smokers were allowed ad libitum food intake in a metabolic ward, 1 wk in CS ph ase and 1 wk in non-CS phase, followed by 4 wk of outpatient non-CS an d a repeat 7-day study. De novo hepatic lipogenesis (DNL), lipolysis, substrate cycling of free fatty acids (FFA), hepatic glucose productio n, and energy expenditure were measured by using a multiple stable-iso tope infusion protocol and indirect calorimetry. Surplus dietary energ y intake (>150% of predicted energy needs) occurred in five of eight s ubjects (2 subjs >5,500 kcal/day, 3 subjs >4,000 kcal/day) with weight gain of 1-4 kg/wk, but with no difference between CS and non-CS phase s. Acute CS significantly increased (P < 0.05) serum FFA concentration s (58%), FFA flux (63%), and glycerol flux (36%); nonsignificantly inc reased extra-adipocyte (hepatic) esterification of FFA (125%, P = 0.10 ) and resting energy expenditure (4.1%, P = 0.22); and did not change adipocyte reesterification of FFA or whole body oxidation of fat. Basa l metabolic parameters (after overnight abstention from CS) did not di ffer between phases. Fractional DNL correlated significantly with exce ss energy intake (r(2) = 0.39) and with percentage of total energy nee ds provided by carbohydrate (r(2) = 0.47). The absence or presence of CS did not affect the increase in fractional DNL in subjects with exce ss energy intake, however. We conclude that cessation of CS does not r esult in a rebound tendency to synthesis or storage of fat, even in th e presence of positive short-term energy balance, contrary to previous suggestions. Moreover, stimulation of lipolysis by CS does not increa se oxidation of fat and thereby protect against fat deposition under c onditions of surplus energy intake. The prevention of weight gain afte r cessation of CS, whether or not nicotine is provided, should focus o n energy balance (calorigenesis as well as intake) rather than specifi c alterations in lipid metabolism.