Effect of different protein sources on satiation and short-term satiety when consumed as a starter.

BACKGROUND: Because the source of protein may play a role in its satiating effect, we investigated the effect of different proteins on satiation and short-term satiety. METHODS: Two randomized single-blind cross-over studies were completed. In the first study, we investigated the effect of a preload containing 20 g of casein, whey, pea protein, egg albumin or maltodextrin vs. water control on food intake 30 min later in 32 male volunteers (25 ± 4 yrs, BMI 24 ± 0.4 kg/m(2)). Subjective appetite was assessed using visual analogue scales at 10 min intervals after the preload. Capillary blood glucose was measured every 30 min during 2 hrs before and after the ad libitum meal. In the second study, we compared the effect of 20 g of casein, pea protein or whey vs. water control on satiation in 32 male volunteers (25 ± 0.6 yrs, BMI 24 ± 0.5 kg/m(2)). The preload was consumed as a starter during an ad libitum meal and food intake was measured. The preloads in both studies were in the form of a beverage. RESULTS: In the first study, food intake was significantly lower only after casein and pea protein compared to water control (P = 0.02; 0.04 respectively). Caloric compensation was 110, 103, 62, 56 and 51% after casein, pea protein, whey, albumin and maltodextrin, respectively. Feelings of satiety were significantly higher after casein and pea protein compared to other preloads (P < 0.05). Blood glucose response to the meal was significantly lower when whey protein was consumed as a preload compared to other groups (P < 0.001). In the second study, results showed no difference between preloads on ad libitum intake. Total intake was significantly higher after caloric preloads compared to water control (P < 0.05). CONCLUSION: Casein and pea protein showed a stronger effect on food intake compared to whey when consumed as a preload. However, consuming the protein preload as a starter of a meal decreased its impact on food intake as opposed to consuming it 30 min before the meal.

High plasma leptin is not associated with higher bone mineral density in insulin-resistant premenopausal obese women.

Obesity's protective effect on bone density may be mediated through increased muscle mass, fat mass, increased estrogen, and possibly insulin and leptin levels. To determine the impact of leptin and insulin on bone metabolism, we studied 48 obese normally cycling premenopausal women (age, 31 +/- 10 yr; body mass index, 35.7 +/- 5 kg/m2): 28 insulin resistant (IR) and 20 insulin sensitive (IS) by McAuley index. Anthropometric, body composition, and bone mineral density (BMD) measurements were made, and serum leptin, insulin, free testosterone, IGF-I, bone remodeling markers, and calciotropic hormones were measured. Anthropometric, lifestyle, and biochemical markers were similar in the two groups. Despite higher circulating insulin and leptin levels, IR subjects had similar mean values of serum osteocalcin but higher C-telopeptide (P = 0.052). They had similar BMD at all skeletal sites compared with IS subjects. In the IR group, fat mass but not lean mass, serum leptin, insulin, testosterone, and IGF-I levels correlated positively with hip and/or total-body bone density with R varying between 0.38 and 0.65; no correlations were observed at the spine. Conversely, in the IS group, lean mass, but not fat mass, and only IGF-I correlated with hip BMD/total-body bone mineral content. In conclusion, there is a dichotomy in the impact of body composition parameters and insulin and leptin levels on bone parameters in obese individuals. The interaction between the fat-related endocrine system and bone seems to be complex and may be modulated by local resistance to the putative protective effect of insulin and leptin on bone.

Physiology of food intake regulation: interaction with dietary components.

Food intake is regulated in both the short- and long-term by a complex physiological system that involves neuroendocrine pathways that are both distinct and overlapping. The underlying causes and mechanisms of the dysregulation of food intake in obesity is poorly understood; however, it is clear that dietary components interact with the physiological determinants of food intake and can cause profound alterations during the development of control mechanisms. The objective of this review is to discuss possible food solutions to the obesity epidemic based on our current understanding of food intake regulation and its interaction with dietary components. First, the physiology of long- and short-term food intake regulation is reviewed. The effects of dietary components on food intake, satiety and intake regulatory markers are then discussed with particular emphasis on macronutrient class and source. Finally, the impact of nutritional manipulations during the early stages of development on food intake and metabolic regulation is examined, followed by a brief description of the possible genetic and epigenetic mechanisms involved.