Exploration of nutritional and bioactive peptide properties in goat meat from various primal cuts during in vitro gastrointestinal digestion and absorption.

OBJECTIVE: This research aims to explore the nutritional and bioactive peptide properties of goat meat taken from various primal cuts, including the breast, shoulder, rib, loin, and leg, to produce these bioactive peptides during in vitro gastrointestinal (GI) digestion and absorption. METHODS: The goat meat from various primal cuts was obtained from Boer goats with an average carcass weight of 30±2 kg. The meat was collected within 3 h after slaughter and was stored at -80°C until analysis. A comprehensive assessment encompassed various aspects, including the chemical composition, cooking properties, in vitro GI digestion, bioactive characteristics, and the bioavailability of the resulting peptides. RESULTS: The findings indicate that the loin muscles contain the highest protein and essential amino acid composition. When the meats were cooked at 70°C for 30 min, they exhibited distinct protein compositions and quantities in the sodium dodecyl sulfate-polyacrylamide gel electrophoresis profile, suggesting they served as different protein substrates during GI digestion. Subsequent in vitro simulated GI digestion revealed that the cooked shoulder and loin underwent the most significant hydrolysis during the intestinal phase, resulting in the strongest angiotensin-converting enzyme (ACE) and dipeptidyl peptidase-IV (DPP-IV) inhibition. Following in vitro GI peptide absorption using a Caco-2 cell monolayer, the GI peptide derived from the cooked loin demonstrated greater bioavailability and a higher degree of ACE and DPP-IV inhibition than the shoulder peptide. CONCLUSION: This study highlights the potential of goat meat, particularly cooked loin, as a functional meat source for protein, essential amino acids, and bioactive peptides during GI digestion and absorption. These peptides promise to play a role in preventing and treating metabolic diseases due to their dual inhibitory effects on ACE and DPP-IV.

Physicochemical, Rheological, In-Vitro Digestibility, and Emulsifying Properties of Starch Extracted from Pineapple Stem Agricultural Waste.

In this study, the physicochemical, rheological, in vitro starch digestibility, and emulsifying properties of starch extracted from pineapple stem agricultural waste were investigated in comparison with commercial cassava, corn, and rice starches. Pineapple stem starch had the highest amylose content (30.82%), which contributed to the highest pasting temperature (90.22 °C) and the lowest paste viscosity. It had the highest gelatinization temperatures, gelatinization enthalpy, and retrogradation. Pineapple stem starch gel had the lowest freeze-thaw stability, as evidenced by the highest syneresis value of 53.39% after five freeze-thaw cycles. Steady flow tests showed that pineapple stem starch gel (6%, w/w) exhibited the lowest consistency coefficient (K) and the highest flow behavior index (n), while dynamic viscoelastic measurements gave the gel strength in the following order: rice > corn > pineapple stem > cassava starch gel. Interestingly, pineapple stem starch provided the highest slowly digestible starch (SDS) (48.84%) and resistant starch (RS) (15.77%) contents compared to other starches. The oil-in-water (O/W) emulsion stabilized with gelatinized pineapple stem starch exhibited higher emulsion stability than that stabilized with gelatinized cassava starch. Pineapple stem starch could therefore be used as a promising source of nutritional SDS and RS, and as an emulsion stabilizer for food applications.

Diet-induced obesity enhances postprandial glucagon-like peptide-1 secretion in Wistar rats, but not in diabetic Goto-Kakizaki rats.

Glucagon-like peptide-1 (GLP-1) is postprandially secreted from enteroendocrine L-cells and enhances insulin secretion. Currently, it is still controversial whether postprandial GLP-1 responses are altered in obesity and diabetes. To address the issue and to find out possible factors related, we compared postprandial GLP-1 responses in normal rats and in diabetic rats chronically fed an obesogenic diet. Male Wistar rats and diabetic Goto-Kakizaki (GK) rats were fed either a control diet or a high-fat/high-sucrose (HFS, 30 % fat and 40 % sucrose) diet for 26 weeks. Meal tolerance tests were performed for monitoring postprandial responses after a liquid diet administration (62·76 kJ/kg body weight) every 4 or 8 weeks. Postprandial glucose, GLP-1 and insulin responses in Wistar rats fed the HFS diet (WH) were higher than Wistar rats fed the control diet (WC). Although GK rats fed the HFS diet (GH) had higher glycaemic responses than GK rats fed the control diet (GC), these groups had similar postprandial GLP-1 and insulin responses throughout the study. Jejunal and ileal GLP-1 contents were increased by the HFS diet only in Wistar rats. Furthermore, mRNA expression levels of fatty acid receptors (Ffar1) in the jejunum were mildly (P = 0·053) increased by the HFS diet in Wistar rats, but not in GK rats. These results demonstrate that postprandial GLP-1 responses are enhanced under an obesogenic status in normal rats, but not in diabetic rats. Failure of adaptive enhancement of GLP-1 response in GK rats could be partly responsible for the development of glucose intolerance.

What Is GLP-1 Really Doing in Obesity?

Glucagon-like peptide-1 (GLP-1) is a gastrointestinal hormone released in response to meal ingestion and enhances insulin secretion from pancreatic ß cells. In several human studies, GLP-1 secretory responses to oral glucose load or a meal were decreased in subjects with obesity, glucose intolerance, or diabetes compared with those in healthy subjects. However, the results of meta-analysis and cohort studies do not necessarily support this concept. Results from animal studies are also inconsistent; in multiple studies, GLP-1 secretory responses to a meal were repeatedly higher in diet-induced obese rats than in control rats. Thus, the postprandial GLP-1 response is not necessarily decreased but rather enhanced during obesity development, which is likely to play a protective role against glucose intolerance.

Enhanced postprandial glucagon-like peptide-1 secretion during obesity development has a protective role against glucose intolerance induction in rats.

Glucagon-like peptide-1 (GLP-1) is an incretin hormone that regulates postprandial glycaemic response by enhancing insulin secretion. We previously demonstrated that the postprandial GLP-1 response was enhanced during the development of diet-induced obesity in rats. However, the physiological relevance of the enhanced GLP-1 response remained unclear. We aimed to determine the role of endogenous GLP-1 during obesity development. Male Sprague-Dawley rats were given either a control diet or a high-fat/high-sucrose (HFS, 30 % fat and 40 % sucrose, weight basis) diet with or without continuous administration of the GLP-1 receptor antagonist, exendin (9-39) (Ex9, 100 µg/d), for 5 weeks. Meal tolerance tests (MTT) were performed to assess postprandial glucose, insulin and GLP-1 responses to a liquid diet administration (15 kcal (63 kJ)/10 ml per kg body weight) every 2 weeks. The AUC of postprandial glucose in the HFS group was similar to the control group in both MTT (P = 0·9665 and P = 0·3475, respectively), whereas AUC of postprandial GLP-1 (after 4 weeks,P = 0·0457) and of insulin (after 2 and 4 weeks, P = 0·0486 and P = 0·0110) was higher in the HFS group compared with the control group. In the Ex9 group, AUC of postprandial glucose (P = 0·0297 and P = 0·0486) was higher along with a lower insulin response compared with the HFS group (P = 0·0564 and P = 0·0281). These results suggest that enhancement of the postprandial GLP-1 response during obesity development has a role in maintaining a normal postprandial glycaemic response. Hence, enhancing endogenous GLP-1 secretion by certain materials could be a potential target for prevention of glucose intolerance.

Continuous feeding of a combined high-fat and high-sucrose diet, rather than an individual high-fat or high-sucrose diet, rapidly enhances the glucagon-like peptide-1 secretory response to meal ingestion in diet-induced obese rats.

OBJECTIVES: Glucagon-like peptide-1 (GLP-1) is secreted by enteroendocrine L-cells in response to nutrient ingestion. To date, GLP-1 secretion in diet-induced obesity is not well characterized. We aimed to examine GLP-1 secretion in response to meal ingestion during the progression of diet-induced obesity and determinewhether a combined high-fat and high-sucrose (HFS) diet, an individual high-fat (HiFat), or a high-sucrose (HiSuc) diet affect adaptive changes in the postprandial GLP-1 response. METHODS: Rats were fed a control, HiFat diet (30% weight), HiSuc diet (40% weight), or HFS (30% fat and 40% sucrose) diet for 5 wk. Meal tolerance tests were conducted to determine postprandial glucose, insulin, and GLP-1 responses to standard (control) diet ingestion every 2 wk. RESULTS: After 5 wk, body weight gain of the HiFat (232.3 ± 7.8 g; P = 0.021) and HFS groups (228.0 ± 7.8; P = 0.039), but not the HiSuc group (220.3 ± 7.9; P = 0.244), were significantly higher than that of the control group (200.7 ± 5.4 g). In meal tolerance tests after 2 wk, GLP-1 concentration was significantly elevated in the HFS group only (17.2 ± 2.6 pM; P < 0.001) in response to meal ingestions, but the HiFat group (16.6 ± 3.7 pM; P = 0.156) had a similar response as the HFS group. After 4 wk, GLP-1 concentrations were similarly elevated at 15min in the HFS (14.1 ± 4.4; P = 0.010), HiFat (13.2 ± 2.0; P < 0.001), and HiSuc (13.0 ± 3.3; P = 0.016) groups, but the HFS (9.8 ± 1.0; P = 0.019) and HiFat (8.3 ± 1.5; P = 0.010) groups also had significant elevation at 30min. CONCLUSIONS: These results demonstrate that the continuous ingestion of excessive fat and sucrose rapidly enhances the GLP-1 secretory response to luminal nutrients, and the HiFat diet may have a potent effect compared with the HiSuc diet on GLP-1 secretory responses. The increment of postprandial GLP-1 and insulinsecretion may have a role in normalizing postprandial glycaemia and slowing the establishment of glucose intolerance.